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We introduce an approach for calculating perturbative corrections to the ring-polymer instanton approximation to tunneling splittings (RPI+PC) by computing higher-order terms in the asymptotic expansion in ℏ. The resulting method goes beyond standard instanton theory by using information on the third and fourth derivatives of the potential along the tunneling path to include additional anharmonic effects. This leads to significant improvements both in systems with low barriers and in systems with anharmonic modes. We demonstrate the applicability of RPI+PC to molecular systems by computing the tunneling splitting in full-dimensional malonaldehyde and a deuterated derivative. Comparing to both experiment and recent quantum mechanical benchmark results, we find that our perturbative correction reduces the error from −11% to 2% for hydrogen transfer and performs even better for the deuterated case. This makes our approach more accurate than previous calculations using diffusion Monte Carlo and path-integral molecular dynamics while being more computationally efficient. [ABSTRACT FROM AUTHOR]

Quantifying reactive aldehyde biomarkers, such as malondialdehyde, acrolein, and crotonaldehyde, is the most preferred approach to determine oxidative stress. However, reported analytical methods lack specificity for accurately quantifying these aldehydes as certain methodologies may produce false positive results due to harsh experimental conditions. Thus, in this research work, a novel HILIC-MS/MS method with endogenous histidine derivatization is developed, which proves to have higher specificity and reproducibility in quantifying these aldehydes from the biological matrix. To overcome the reactivity of aldehyde, endogenous histidine is used for its derivatization. The generated adduct is orthogonally characterized by NMR and LC-HRMS. The method employed a hydrophilic HILIC column and multiple reaction monitoring (MRM) to accurately quantify these reactive aldehydes. The developed method is an unequivocal solution for quantifying stress in in vivo and in vitro studies. [ABSTRACT FROM AUTHOR]

Bell pepper is a major vegetable crop of global commercial interest, but the postharvest quality is constrained by faster deterioration and senescence. Brassinosteroids (BRs), are an emerging and novel biomolecule that delay ripening and senescence in various vegetables. Freshly harvested bell pepper fruit were immersed in an aqueous solution of BRs concentrations (0, 2, 5, 7 and 10 μM) for 20 min and subsequently stored for 20 d at 10 ± 1°C, 85–90% RH. The bell pepper treated with 10 μM BRs significantly reduced respiration rate (∼2.3 fold), delayed weight loss (∼2.2 fold), and retained higher firmness (∼2.5 fold), total phenolic (∼1.7 fold), flavonoid (∼1.7 fold), proline (∼2 fold) and ascorbic acid content (∼2 fold) over the control fruit at the end of cold storage. Also, it retained higher DPPH radical scavenging (∼1.8 fold) and antioxidant enzyme activity (∼1.5 fold) over the control at the end of cold storage. Moreover, BRs treated bell pepper exhibited reduced malondialdehyde accumulation and delayed capsaicin, and chlorophyll degradation. Remarkably, 10 μM BRs treatment prolonged the shelf-life of bell pepper up to 20 d (10 d extra over control) without compromising quality and sensory acceptability. [Display omitted] • Brassinosteroid (10 µM L–1) was found most effective treatment in maintaining the quality and shelf life of bell pepper. • BRs suppressed respiration, color alteration, chlorophyll degradation and weight loss. • BRs retained higher firmness, bioactive compounds, and antioxidant enzymes and reduced MDA accumulation. • BRs enhanced the shelf life of bell pepper by 20 d with superior sensory quality. [ABSTRACT FROM AUTHOR]

Guava fruit is an abundant source of phytonutrients namely, vitamin C, carotenoids, minerals and polyphenols. However, due to its climacteric nature, fruit are highly perishable and susceptible to low temperature storage resulting in poor shelf life. The current investigation emphasizes the antioxidant potential of melatonin (MT) on ripening and quality of guava (cv. Barafkhana) fruit during cold storage. Physiologically mature fruit were immersed in MT solutions (200, 400, 600, and 800 μmol L−1) for 30 min at 20 ± 2 °C. Subsequently, the fruit were stored in cold storage at 10 ± 1 °C and 85–90 % relative humidity for 20 days. In results, MT at 600 μmol L−1 significantly suppressed the ethylene evolution and respiration rate, and reduced weight loss, while retaining firmness. Also, higher levels of total soluble solids, total sugars and total chlorophyll were retained in MT treated fruit over control. Bioactive compounds such as ascorbic acid, total phenols, flavonoids and antioxidant activity were high in fruit subjected to MT treatment. Furthermore, exogenous MT application prevented the accumulation of malondialdehyde and hydrogen peroxide, indicating a potential inhibition of reactive oxygen species (ROS) burst and oxidative damage. Moreover, MT application boosted the scavenging capacity of ROS by enhancing the activities of superoxide dismutase, catalase, guaiacol peroxidase, and ascorbate peroxidase. The multivariate statistical approaches such as principal component analysis and Pearson's correlation coefficient also confirmed that MT (600 μmol L−1) is a potential novel phytohormone to preserve the sensory quality of guava fruit during cold storage via stimulating antioxidant system. [Display omitted] • Postharvest melatonin (MT) application (600 μmol L−1) preserved quality of stored guava fruit up to 20 days. • Delayed fruit senescence, suppressed ethylene production and respiration rates and retained firmness, TSS and chlorophyll. • MT alleviated oxidative stress and preserved cell membrane integrity. • MT stimulated the antioxidant system via enhancing the antioxidant enzyme activities (SOD, CAT, APX and GPX). [ABSTRACT FROM AUTHOR]

This study investigated the effects of ghrelin on oxidative stress, working memory, inflammatory parameters, and neuron degeneration. TBI was produced with the weight-drop technique. Rats in the G+TBI and TBI+G groups received ghrelin for 7 or 2 days, respectively. The control group received saline. On the 8th day of the study, the brain and blood tissue were taken under anesthesia. A significant increase in brain GSH-PX, MDA, IL-1β, TGF-β1, and IL-8 levels and a significant decrease in CAT levels were found in the TBI group compared to the control. Serum MDA, GSH, IL-1β, and IL-8 levels were increased with TBI. Ghrelin treatment after TBI significantly increased the serum GSH, CAT, GSH-PX, and brain GSH and CAT levels, while it significantly decreased the serum MDA, IL-1β, and brain MDA, TGF-β1, and IL-8 levels. Histological evaluations revealed that ghrelin treatment led to a reduction in inflammation, while also significantly ameliorating TBI-induced neuron damage and vascular injuries. Immunohistochemistry staining showed that GFAP staining intensity was significantly increased in the cortex and hippocampus in TBI, and GFAP immunoreactivity was decreased with ghrelin treatment. The results from this study suggested that ghrelin may have curative effects on TBI. [ABSTRACT FROM AUTHOR]

Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a crucial role in ferroptosis by regulating the cellular antioxidant response and maintaining redox balance. However, compounds that induce ferroptosis through dual antioxidant pathways based on Nrf2 have not been fully explored. In our study, we investigated the impact of Gambogic acid (GA) on MCF-7 cells and HepG2 cells in vitro. The cytotoxicity, colony formation assay and cell cycle assay demonstrated potent tumor-killing ability of GA, while its effect was rescued by ferroptosis inhibitors. Furthermore, RNA sequencing revealed the enrichment of ferroptosis pathway mediated by GA. In terms of ferroptosis indicators detection, evidences for GA were provided including reactive oxygen species (ROS) accumulation, alteration in mitochondrial membrane potential (MMP), disappearance of mitochondrial cristae, lipid peroxidation induction, malondialdehyde (MDA) accumulation promotion, iron ion accumulation as well as glutathione (GSH)/thioredoxin (Trx) depletion. Notably, Ferrostatin-1 (Fer-1) and Liproxstatin-1 (Lip-1) successfully rescued GA-induced MDA accumulation. In terms of mechanism, Nrf2 was found to play a pivotal role in GA-induced ferroptosis by inducing protein alterations through the iron metabolism pathway and GSH/Trx dual antioxidant pathway. Furthermore, GA exerted good antitumor activity in vivo through GSH/Trx dual antioxidant pathway, and Fer-1 significantly attenuated its efficacy. In conclusion, our findings first provided new evidence for GA as an inducer of ferroptosis, and Nrf2-mediated GSH/Trx dual antioxidant system played an important role in GA-induced ferroptosis. [Display omitted] • GA exhibited its anticancer activity by inducing ferroptosis in vitro and in vivo. • Nrf2 played an important role in GA-induced ferroptosis. • GSH/Thioredoxin dual antioxidant system was first found to induce ferroptosis. [ABSTRACT FROM AUTHOR]

Methylene blue (MB) has a long story of use and has been employed for various diseases, however, most of its current rekindled research is related to its function in the mitochondria. MB is gaining interest as a possible treatment because mitochondrial dysfunction is an apparent unifying pathogenic characteristic of a variety of neurodegenerative conditions. Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by impairment of cognitive functions. This study aims to investigate whether MB treatment improves impaired cognitive functions and reduces hippocampal amyloid-β levels and oxidative stress in a D-galactose-induced AD mouse model. Twenty-four wild-type Balb/c mice were randomly divided into four groups (control, D-galactose-induced AD, MB-treated AD, and only MB-treated mice). Mice in the corresponding groups were injected with D-galactose (50 mg/kg, s.c.) for 60 days. In the MB treatment groups, the mice were treated with MB (2 mg/kg, orally) for the last 14 days of treatments. The Morris water maze test was used to assess spatial learning and memory functions. Amyloid β-42, malondialdehyde, superoxide dismutase, and nitric oxide levels in the hippocampi of mice were measured using ELISA and spectrophotometry. MB treatment improved impaired learning and memory functions induced by D-galactose administration and decreased amyloid β-42 concentration in the hippocampi of mice. Malondialdehyde level was found to decrease in MB-treated mice compared to D-galactose-induced AD mice in the hippocampus and plasma. The hippocampus of MB-treated mice displayed increased superoxide dismutase activity while decreased nitric oxide concentration compared to the ones of D-galactose-induced AD mice. MB has been shown to improve learning and memory impairments, as well as reduce Aβ-42 concentration and oxidative stress in the hippocampus of D-galactose-induced AD mice. The findings of this study demonstrate that MB may offer potential benefits as a repurposed agent for AD. [ABSTRACT FROM AUTHOR]

Purpose: Polycystic ovary syndrome (PCOS) is an endocrine disorder that primarily affects women of reproductive age. It is recognized as the leading cause of infertility due to anovulation. This research aims to evaluate the diagnostic potential of oxidative stress biomarkers, including advanced oxidation protein products (AOPP), malondialdehyde (MDA), uric acid (UA), and nitric oxide (NO), in identifying PCOS. Methods: A literature search was conducted in the EMBASE, PubMed, Cochrane Library, and Scopus databases. The standardized mean difference (SMD) and 95% confidence interval (CI) were employed to assess the correlation between free radical product and PCOS. Moreover, the presence of heterogeneity among the studies was assessed utilizing the I2 statistic and Cochran Q test. The methodological rigor of the incorporated studies was assessed through the application of the Newcastle-Ottawa Scale. Furthermore, the presence of publication bias was determined via Begg and Egger tests. Results: This meta-analysis reviewed 38 observational studies, including 17,845 women. The results revealed a significant association between PCOS in women and alterations in free radical levels. The study revealed that the PCOS group had significantly higher levels of AOPP (SMD = 3.193; 95% CI, 2.86 to 3.25), UA (SMD = 0.68; 95% CI, 0.24 to 1.13), and MDA (SMD = 1.16; 95% CI, 0.77 to 1.56) compared to the healthy control group. Furthermore, the analysis found a significantly lower level of NO (SMD = (− 0.59); 95% CI, − 1.15 to − 0.03) in the PCOS patient. Conclusion: Screening of specific biomarkers associated with free radical products could provide valuable benefits in the prognosis and diagnosis of PCOS. [ABSTRACT FROM AUTHOR]

Rationale: Malondialdehyde, one of the peroxidation products of polyunsaturated fatty acids, has been widely reported as an oxidative stress biomarker in many diseases. However, malondialdehyde is inherently unstable in biological matrices, which renders its measurement unreliable with all the reported analytical methods. To find an alternative oxidative stress biomarker, we envisioned that N‐(2‐carboxyethyl)proline, a modified conjugate of malondialdehyde and proline, could be a stable candidate for this purpose. Methods: The proposed compound was chemically synthesized, and liquid chromatography–mass spectrometry methods were developed and used to search for the compound in human biological samples. Results: An endogenous metabolite in human feces and urine samples was found to match the synthetic N‐(2‐carboxyethyl)proline by chromatographic retention and the fragmentation pattern of its molecular ion. Conclusion: The results confirmed that N‐(2‐carboxyethyl)proline was a new metabolite in human feces and urine samples. In addition, our results demonstrated a case of successful identification of true unknown metabolite by knowledge‐based hypothesis of possible metabolites followed by experimental confirmation with a synthetic standard. [ABSTRACT FROM AUTHOR]

The objective of this study was to examine the effects of enriching the diet with Omega-3 fatty acids on the productive performance, yolk fatty acid profiles, oxidative stability, blood biochemistry, and immune system of laying hens. Enriching the diet with Omega-3 improved egg production and FCR (P < 0.05). Docosahexaenoic acid (DHA) and total omega-3 fatty acids in the yolk increased linearly with Salomega level (P < 0.05). Serum cholesterol and triglyceride decreased, but HDL content increased parallel to the Salomega level in the diet (P < 0.05). The MDA level in the yolk of bird eggs of the 3 or 4% Salomega treatment was higher than the MDA level of the control group (P < 0.05). In conclusion, the enrichment of laying hens’ diet with 3 and 4% salomega can enhance egg production, elevate the levels of Omega-3 fatty acids, and decrease the oxidative stability of yolk lipids. [ABSTRACT FROM AUTHOR]

Background. Preeclampsia (PE) is a common obstetric disorder hallmarked by impaired trophoblast invasion and a skew toward an inflammatory immune response. Echinatin, a flavonoid with established anti-inflammatory, antioxidant, and anticancer activities, may offer therapeutic benefits in PE. Our study aimed to investigate the effect of echinatin on preeclampsia in vitro and in vivo and to reveal the potential molecular mechanism of its action. Methods. Eighteen adult female Sprague Dawley rats were randomized into three experimental groups: a PE model group, a PE + echinatin treatment group, and a PE + echinatin treatment group with TLR4 overexpression. Placental tissue CK7 expression was assessed by immunohistochemistry. TUNEL immunofluorescence staining quantified placental cell apoptosis. Cell viability, proliferation, and migration were evaluated using cell counting kit-8, EdU incorporation, and Transwell assays, respectively. Oxidative stress parameters of malondialdehyde, superoxide dismutase, and glutathione peroxidase were measured. Flow cytometry determined cell apoptosis and intracellular reactive oxygen species (ROS) levels. Western blotting evaluated the expression of proteins related to the TLR4-MyD88-NF-κB signaling pathway, and the concentrations of TNF-α, IL-6, and IL-18 were measured with ELISA kits. Results. Echinatin mitigated placental damage, reduced apoptosis, and increased CK7 expression. It significantly enhanced HTR-8/SVneo cell viability and migration. Echinatin also counteracted H2O2-induced ROS production and cell death in HTR-8/SVneo cells. Moreover, it inhibited the expression of proteins within the TLR4-MyD88-NF-κB signaling cascade. Overexpression of TLR4 negated echinatin's protective effects. Conclusion. Echinatin exerts protective effects against oxidative stress and inflammation in PE by targeting the TLR4-MyD88-NF-κB pathway, suggesting its therapeutic potential for the management of preeclampsia. [ABSTRACT FROM AUTHOR]

Background: Numerous studies have investigated the correlation between malondialdehyde (MDA) and cognitive decline. However, limited research has explored the interplay between superoxide dismutase (SOD), C-reactive protein (CRP), and MDA. Objective: This study aims to scrutinize the association between MDA and cognitive function in older adults, while also elucidating the roles of SOD and CRP within this relationship. Methods: Utilizing data from the Chinese Longitudinal Healthy Longevity Survey (CLHLS) spanning 2008–2009, 2011–2012, and 2014, this study included 2,696 eligible subjects. Cognitive function was evaluated using the Chinese version of the Mini-Mental State Examination (MMSE). Linear mixed-effects models were employed to examine the links between MDA, SOD, CRP, and their interactions with cognitive function. Results: Elevated serum levels of MDA and CRP, as well as decreased serum SOD levels, were related to decreased cognitive function (β= –0.220 and –0.346, 95% CI: –0.399, –0.041 and –0.526, –0.167 for MDA and CRP; β= 0.384, 95% CI: 0.204, 0.564 for SOD). Notably, a significant interaction between MDA and SOD was detected (p = 0.001). An increase per standard deviation in serum MDA levels was significantly associated with a 0.347-point lower MMSE score only in participants with normal cognitive function and high SOD levels (β= –0.347, 95% CI: –0.497, –0.197; p < 0.001). Conclusions: Elevated serum MDA levels in the normal population with high SOD levels suggested diminished cognitive performance. Combining MDA with SOD could be pivotal in identifying older adults at risk of cognitive decline in clinical settings. [ABSTRACT FROM AUTHOR]

Objective: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among women of reproductive age and is one of the main causes of ovulation infertility, affecting 5-10% of women. Inflammation, hormonal imbalances, and disruption of the oxidant-antioxidant balance are the main factors in the pathophysiology of PCOS. This study was designed to answer the question of whether apigenin and chrysin have therapeutic effects on the dehydroepiandrosterone (DHEA)-induced rat model of PCOS. Materials and Methods: The experimental PCOS model was created by administering 6 mg/100g DHEA subcutaneously to 21-day-old female Wistar rats for 28 days, followed by treatment with natural agents 50 mg/kg apigenin and 50 mg/kg chrysin by oral gavage twice a week for one month. The predominant cell type was determined by microscopic analysis in vaginal smears daily from day 10 to day 28 of the experiment. In tissue supernatants, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, and malondialdehyde (MDA) levels were obtained by spectrophotometric method with appropriate manual methods; follicle-stimulating hormone (FSH), luteinizing hormone (LH), progesterone, interleukin (IL)-18, IL-1β, and IL-13 levels were determined by enzyme-linked immunosorbent assay (ELISA) method. In addition, histological sections obtained from ovarian tissue samples were stained with hematoxylin-eosin and examined under a light microscope. Results: The results showed that treatment with apigenin and chrysin alone and in combination reduced MDA, LH, FSH, progesterone, IL-1β, IL-13, and IL-18 levels compared with PCOS rats. Furthermore, enzymatic activities of antioxidants including CAT, SOD, and GPx in the ovaries increased in therapeutic groups compared to the PCOS group. Conclusion: In conclusion, this study demonstrates the potential therapeutic efficacy of apigenin and chrysin, either alone or in combination, in alleviating the hormonal imbalances, inflammation, and oxidative stress in DHEA-induced PCOS rats. Apigenin, in particular, emerges as a promising agent for PCOS treatment, showing superiority over chrysin and combination treatments in ameliorating cystic follicles and improving various parameters associated with PCOS pathophysiology. These findings suggest that apigenin holds promise as a novel therapeutic agent for PCOS and warrants further investigation in clinical settings. [ABSTRACT FROM AUTHOR]

BACKGROUND: Minimizing food oxidation remains a challenge in several environments. The addition of rosemary extract (150 mg kg−1) and lyophilized parsley (7.1 g kg−1) at equivalent antioxidant activity (5550 μg Trolox equivalents kg−1) to meat patties was assessed in terms of their effect during microwave cooking and after being subjected to an in vitro digestion process. RESULTS: Regardless of the use of antioxidants, cooking caused a decrease of the fat content as compared to raw samples, without noticing statistical differences in the fatty acid distribution between raw and cooked samples [44%, 47% and 6.8%, of saturated fatty acid (SFA), monounsaturated fatty acid (MUFA) and polyunsaturated fatty acid (PUFA), respectively]. However, the bioaccessible lipid fraction obtained after digestion was less saturated (around 34% SFA) and more unsaturated (35% MUFA +30% PUFA). Cooking caused, in all types of samples, an increased lipid [thiobarbituric acid reactive substances (TBARS)] and protein (carbonyls) oxidation values. The increase of TBARS during in vitro digestion was around 7 mg malondialdehyde (MDA) kg−1 for control and samples with parsley and 4.8 mg MDA kg−1 with rosemary. The addition of parsley, and particularly of rosemary, significantly increased the antioxidant activity (DPPH) of cooked and digested microwaved meat patties. CONCLUSION: Whereas rosemary was effective in minimizing protein oxidation during cooking and digestion as compared to control samples, parsley could only limit it during digestion. Lipid oxidation was only limited by rosemary during in vitro digestion. © 2024 The Authors. Journal of The Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Background: Paclitaxel (PAX) is a widely used chemotherapy drug for various cancer types but often induces significant toxicity in multiple organ systems. Silymarin (SIL), a natural flavonoid, has shown therapeutic potential due to its multiple benefits. Aims: To evaluate the therapeutic efficacy of SIL in mitigating liver and kidney damage induced by PAX in rats, focusing on oxidative stress, inflammation, and apoptosis pathways. Study Design: Experimental animal model. Methods: The study included 28 male Wistar rats aged 12-14 weeks weighing 270-300 g. The rats were divided into four groups: control, SIL, PAX, and PAX + SIL, with seven in each group. The rats received intraperitoneal (i.p.) injections at a dose of 2 mg per kilogram of body weight of PAX for 5 successive days, followed by oral gavage with 200 mg/ kg body mass of SIL for 10 uninterrupted days. We examined the effect of SIL on specific serum biochemical parameters using an autoanalyzer and rat-specific kits. The spectrophotometric methods was used to investigate oxidative stress indicators in kidney and liver tissues. Aquaporin-2 (AQP-2), B-cell lymphoma-2 (Bcl-2), cysteine aspartate-specific protease-3 (caspase-3), interleukin-6 (IL-6), nuclear factor kappa B (NF-κB), and streptavidin-biotin staining were used to assess immunoreactivity in PAX-induced liver and kidney injury models. Results: SIL treatment significantly reduced serum levels of alanine aminotransferase, aspartate aminotransferase, creatinine, urea, and C-reactive protein, indicating its effectiveness in treating PAX-induced liver and kidney injury. SIL treatment significantly reduced oxidative stress by increasing essential antioxidant parameters, such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione. It also reduced malondialdehyde levels in liver and kidney tissues of SIL-PAX groups (p < 0.05). SIL administration reduced NF-κB, caspase-3, and IL-6 expression while increasing Bcl-2 and AQP2 levels in liver and kidney tissues of rats treated with SIL and PAX (p < 0.05). Conclusion: Our findings indicate the potential of SIL to alleviate PAX-induced liver and kidney damage in rats by reducing oxidative stress, inflammation, and apoptotic processes. [ABSTRACT FROM AUTHOR]

Objectives: The objective of the study was to evaluate whether a twice‐daily instillation of 0.45% preservative‐free ketorolac tromethamine (FKT) or 0.4% benzalkonium chloride‐preserved ketorolac tromethamine (BACKT), every 12 h for 30 days may affect tear film parameters and the meibography in healthy dogs. Additionally, we assessed whether the same treatments irritated the ocular surface, affected goblet cell density (GCD), and the levels of oxidative stress biomarkers (OSB) in the conjunctiva of the same dogs. Procedures: Experimental and masked comparison study. In 11 healthy dogs baseline values of the lipid layer thickness, tear meniscus height, non‐invasive tear breakup time (NI‐TFBT), and the meibomian gland (MG) loss were assessed by OSAvet®. For each dog, one eye received 40 μL of BACKT, while the other received 40 μL FKT, every 12 h for 30 consecutive days. Tear parameters and meibography were repeated 15, 30, and 60 days post‐treatments. Conjunctival hyperemia and blepharospasm were monitored at the same time points. At baseline and Day 30, a conjunctival biopsy was collected for GCD and OSB determination. Results: Conjunctival hyperemia and blepharospasm were not observed. At Day 15, the MG loss increased only in FKT‐treated eyes (p <.001). On Day 30, both treatment groups showed increased MG loss, shortened NI‐TFBT, and reduced GCD and catalase (p <.05). At Day 30, BACKT‐treated eyes showed lower levels of superoxide dismutase (SOD) (p =.006) and higher levels of malondialdehyde (MDA) (p =.02). Differences between treatments were not observed for any parameter at any time point (p >.05). 60 days after treatment, OSAvet® parameters tended to return to values assessed at baseline; however, significant differences remained for MG loss (p <.05). Conclusions: Twice‐daily instillation of KT, containing or not BAC, for 30 consecutive days shortened NI‐TFBT, decreased GCD, and increased the MG loss in healthy dogs. KT should be used with caution when prescribed for long periods, particularly in patients with tear film abnormalities. However, future controlled studies using KT, BAC, and other topical NSAIDs are indicated to further support this finding. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease, a disease featured by intestinal epithelial barrier destruction and dysfunction, has been a constant threat to animal health. The primary objective of this research was to assess the impact of the extract derived from lotus leaves (LLE) on lipopolysaccharide (LPS) induced damage to the intestines in mice, as well as to investigate the fundamental mechanism involved. The LLE was prepared using ultrasonic extraction in this experiment, and the LLE total flavonoid content was 117.02 ± 10.73 mg/g. The LLE had strong antioxidant activity in vitro, as assessed by 2, 2-diphenyl-1-picrylhydrazyl, ferric reducing antioxidant power, and 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) methods. In the vivo experiment, different doses of LLE (50, 100, and 200 mg/kg) were administered for 2 weeks before LPS treatment in mice. The results revealed that LLE alleviates intestinal tissue damage in LPS-induced mice. In the jejunum tissue, LLE significantly upregulated mRNA and protein expression levels of tight junction proteins, such as ZO-1, occludin, and claudin-1, and decreased the contents of the inflammatory cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. Furthermore, the malondialdehyde and lactate dehydrogenase contents increased by LPS in the liver were significantly reduced after administration of LLE, and the total antioxidant capacity, superoxide dismutase, and reduced glutathione decreased by LPS were remarkably increased by LLE. It was found that LLE could relieve LPS-induced oxidative stress by upregulating mRNA and protein expression of Nrf2 and HO-1 in jejunum tissue. In conclusion, LLE alleviates LPS-induced intestinal damage through regulation of the Nrf2/HO-1 signal pathway to alleviate oxidative stress, reducing inflammatory factors and increasing the expression of tight junction proteins in mice. [ABSTRACT FROM AUTHOR]

This research investigated the antioxidant responses of Pleurotus florida at different concentrations of gas oil [0% (control), 2.5%, 5%, and 10% (v:v)] for 30 days. The activities of superoxide dismutase and catalase enzymes decreased in responses to the gas oil presence by an average of 83% and 49%, respectively. In contrast, the activities of the ascorbate peroxidase and glutathione peroxidase enzymes displayed an upward trend in the groups cultured in oil-contaminated media. The gas oil contaminant increased total phenol and flavonoid accumulation, reflecting the variation in secondary metabolism. According to the 1,2-diphenyl-2-picrylhydrazyl radical scavenging, the 2.5% gas oil treatment resulted in the highest antioxidant activity (48 μg mL−1). The highest scavenging activity of nitric oxide radicals (IC50 = 272 μg mL−1) was observed in the treatment with the highest gas oil concentration (10%). Also, this treatment showed an excellent ability to chelate Fe+2 ions (IC50 = 205 μg mL−1). The IC50 values of methanolic extract for nitric oxide scavenging activity and metal chelating ability were significantly reduced by increasing gas oil concentration in the treatments. With increasing the gas oil concentration, malondialdehyde content as a criterion measure of lipid peroxidation level showed significant reduction. These results show that P. florida is resistant to and a compatible mushroom with oil pollutants. Also, the activity of glutathione peroxidase and the ascorbate-glutathione cycle detoxify nitric oxide radicals and products of reactive oxygen species–induced lipid peroxidation in the gas oil treatments. [ABSTRACT FROM AUTHOR]

Here, we describe GS-9, a novel water-soluble fatty acid-based formulation comprising L-lysine and arachidonic acid, that we have shown to induce ferroptosis. GS-9 forms vesicle-like structures in solution and mediates lipid peroxidation, as evidenced by increased C11-BODIPY fluorescence and an accumulation of toxic malondialdehyde, a downstream product of lipid peroxidation. Ferroptosis inhibitors counteracted GS-9-induced cell death, whereas caspase 3 and 7 or MLKL knock-out cell lines are resistant to GS-9-induced cell death, eliminating other cell death processes such as apoptosis and necroptosis as the mechanism of action of GS-9. We also demonstrate that through their role of sequestering fatty acids, lipid droplets play a protective role against GS-9-induced ferroptosis, as inhibition of lipid droplet biogenesis enhanced GS-9 cytotoxicity. In addition, Fatty Acid Transport Protein 2 was implicated in GS-9 uptake. Overall, this study identifies and characterises the mechanism of GS-9 as a ferroptosis inducer. This formulation of arachidonic acid offers a novel tool for investigating and manipulating ferroptosis in various cellular and anti-cancer contexts. [ABSTRACT FROM AUTHOR]

The Chinese mitten crab (Eriocheir sinensis) is one of the most commercially important crustacean species in China. The aim of this study was to characterize the toxic effects of butachlor (an herbicide of the acetanilide class) on juvenile E. sinensis crabs. The lethal effects and the acute toxicity of butachlor on juvenile E. sinensis specimens were assessed through a semi-static in vitro experiment. We determined the activities of superoxide dismutase (SOD) and catalase (CAT) as well as the levels of glutathione (GSH) and malondialdehyde (MDA) in the gills and the hepatopancreas of the juvenile crabs, at different time points over a 14-day short-term exposure to butachlor. Moreover, we measured the residual levels of butachlor in three different tissues (gills, hepatopancreas, and muscles) of the juvenile crabs over a longer period. Our findings revealed that butachlor is highly toxic for juvenile E. sinensis crabs. In fact, the median lethal concentration (LC50) values of butachlor at 24, 48, 72, and 96 h were found to be 4.22, 1.84, 0.34, and 0.14 mg/L, respectively, while the safe concentration was 0.014 mg/L. The antioxidant defense ability of the juvenile E. sinensis crabs against butachlor was induced after exposure to the herbicide at a concentration of 0.01 mg/L. After 14 days of exposure to butachlor at 0.04 and 0.16 mg/L, both SOD and CAT were found to be significantly inhibited (p < 0.05), the GSH levels were found to be significantly decreased (p < 0.05) and the MDA levels were identified as significantly increased (p < 0.05). Moreover, after 14 days of exposure to butachlor at 0.16 mg/L, the activities of SOD and CAT as well as the content of GSH in the hepatopancreas were found to be significantly decreased (p < 0.05). Our results revealed that a high concentration of butachlor was capable of inducing oxidative stress and damage in juvenile E. sinensis crabs. The maximal residual value of butachlor was obtained in the gills, with a content of 4.56 μg/kg. Butachlor was not detected after 24 days in the aforementioned three tissues of the juvenile crabs, thereby indicating that it was effectively metabolized. [ABSTRACT FROM AUTHOR]

Summary Melatonin (MT), a natural signalling compound derived from tryptophan, has gained significant attention for delaying postharvest ripening and senescence in various fruits and vegetables. In the present study, the effect of MT treatment was evaluated on the postharvest shelf‐life of bell pepper. Fruits were dipped in various MT concentrations (70, 120, 170, 220 μmol L−1) for 20 min and stored at 10 ± 1 °C for 20 days. The bell pepper treated with 120 μmol L−1 MT significantly suppressed respiration, weight loss and delayed chlorophyll degradation. Additionally, MT (120 μmol L−1) treatment reduced loss of firmness, titratable acidity and retained total phenol, flavonoid and ascorbic acid content. It hindered malondialdehyde accumulation by enhanced DPPH radical scavenging and antioxidant enzyme activity like superoxide dismutase, catalase and peroxidase, over the control. Conclusively, 120 μmol L−1 MT prolongs the postharvest shelf‐life of bell pepper by 20 days with superior sensory quality, surpassing the control by 10 days. Therefore, MT treatment is a commercially useful technology for maintaining quality and prolonging the postharvest shelf‐life of bell pepper. [ABSTRACT FROM AUTHOR]

Bilobalide has shown strong anti-inflammatory activity. Colorectal cancer (CRC) is closely associated with inflammation. However, no studies have reported on the use of bilobalide for treating CRC. This study aims to evaluate the effect of bilobalide on CRC prevention. Enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (RT-qPCR), Western blotting, and immunofluorescence showed that bilobalide significantly inhibits the M2 polarization of macrophages dependent on phorbol 12-myristate 13-acetate (PMA) and interleukin-4 (IL-4). Analysis of signaling pathways showed that the phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and signal transducer and activator of transcription 3 (STAT3) was regulated. In particular, human CRC organoids were established. Western blotting, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL), and analysis of cell viability and morphology further supported the hypothesis that the anti-CRC effects of bilobalide could be explained by its ability to suppress M2 macrophage polarization and promote M1 transformation. C57BL/6 mice treated with azoxymethane (AOM)/dextran sodium sulfate (DSS) were divided into three groups, i.e., control, AOM/DSS, low (2.5 mg/kg), and high (5 mg/kg). High-dose bilobalide markedly inhibited the progression of CRC, as evidenced by the increased body weight, decrease in disease activity index (DAI) death rate, and alleviation of colon length reduction and tumorigenesis. According to the in vivo results, reduced levels of inflammatory cytokines in the serum included tumor necrosis factor (TNF-α), IL-6, IL-1β, and IL-10. Bilobalide reduced oxidative stress indices, lipid peroxide (LPO), and malondialdehyde (MDA) and increased reduced glutathione (GSH). In addition, the expression of proliferating cell nuclear antigen (PCNA), Ki67, cellular Myc (c-Myc), and CD206 was downregulated in the drug-treated groups, as confirmed by the immunohistochemical staining. Collectively, these results indicated that bilobalide administration improve experimental CRC by inhibiting M2 macrophage polarization and oxidative stress. Thus, bilobalide may prevent CRC and serve as a potential therapeutic target for CRC. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) affecting 334 million people in the world remains a major cause of morbidity and mortality. Proper diagnosis of COPD is still a challenge and largely solely based on spirometric criteria. We aimed to investigate the potential of nitrosative/oxidative stress and related metabolic biomarkers in exhaled breath condensate (EBC) to discriminate COPD patients. Methods: Three hundred three participants were randomly selected from a 15,000-transit worker cohort within the Respiratory disease Occupational Biomonitoring Collaborative Project (ROBoCoP). COPD was defined using the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria as post-bronchodilator ratio of Forced Expiratory Volume in 1st second to Forced Vital Capacity < 0.7 in spirometry validated by an experienced pulmonologist. Discriminative power of biomarker profiles in EBC was analyzed using linear discriminant analyses. Results: Amongst 300 participants with validated spirometry, 50.3% were female, 52.3 years old in average, 36.0% were current smokers, 12.7% ex-smokers with mean tobacco exposure of 15.4 pack-years. Twenty-one participants (7.0%) were diagnosed as COPD, including 19 new diagnoses, 12 of which with a mild COPD stage (GOLD 1). Amongst 8 biomarkers measured in EBC, combination of 2 biomarkers, Lactate and Malondialdehyde (MDA) significantly discriminated COPD subjects from non-COPD, with a 71%-accuracy, area under the receiver curve of 0.78 (p-value < 0.001), and a negative predictive value of 96%. Conclusions: These findings support the potential of biomarkers in EBC, in particular lactate and MDA, to discriminate COPD patients even at a mild or moderate stage. These EBC biomarkers present a non-invasive and drugless technique, which can improve COPD diagnosis in the future. [ABSTRACT FROM AUTHOR]

[Objectives] This study was conducted to investigate the scientific prevention and control of Solanum nigrum L. [Methods] Through experiments on S. nigrum from different sources, it was found that glyphosate stress had significant effects on antioxidant enzyme activity and oxidative damage of sensitive S. nigrum plants. [Results] Sensitive S. nigrum showed oxidative damage under glyphosate stress, while resistant S. nigrum responded to adversity damage by improving its antioxidant enzyme activity. The experimental results showed that the antioxidant enzymes and reduced glutathione of S. nigrum had certain metabolic detoxification effects under glyphosate stress. [Conclusions] This study provides a theoretical basis for scientific prevention and control of S. nigrum, and has a certain reference value for revealing the glyphosate resistance mechanism of S. nigrum. [ABSTRACT FROM AUTHOR]

Purpose: This research intended the utilization of Javanese turmeric (0.4% w/v) as a kombucha substrate and analysis of its hepatoprotective activity, in comparison against nonfermented Javanese turmeric beverage (JTB) and black tea kombucha. Design/methodology/approach: Forty-two healthy male Balb/c mice (two- to three-week-old, 20–30 g) were divided into six groups with seven replicates each. The treatments were normal diet, normal diet + Javanese turmeric kombucha (JTK), normal diet + diethylnitrosamine (DEN), DEN + JTB, DEN + JTK, DEN + black tea kombucha. Kombuchas and JTB were given at 0.3 mL/20 g BW/d. DEN was induced intraperitoneally at a dose of 100 mg/kg. Observed biomarkers were blood serum glutamate pyruvate transaminase (SGPT) and serum glutamate oxaloacetate transaminase (SGOT) activity, serum malonaldehyde (MDA), as well as liver histology. Data were analyzed using analysis of variance. Findings: Among DEN-induced groups, JTK significantly (p < 0.05) diminished the level of blood SGPT, SGOT and serum MDA. JTK also had lower blood SGPT (8.604 ± 2.195 U/L) and serum MDA levels (2.884 ± 0.083 nM/mL) compared to the normal group (8.604 ± 2.195 U/L and 5.050 ± 0.998 nM/mL, respectively). JTK also produced the least damaged liver-cell numbers. Originality/value: JTK demonstrated better hepatoprotective activity compared to JTB. [ABSTRACT FROM AUTHOR]

Background: Migraine stands as a prevalent primary headache disorder, with prior research highlighting the significant involvement of oxidative stress and inflammatory pathways in its pathogenesis and chronicity. Existing evidence indicates the capacity of Dl-3-n-butylphthalide (NBP) to mitigate oxidative stress and inflammation, thereby conferring neuroprotective benefits in many central nervous system diseases. However, the specific therapeutic implications of NBP in the context of migraine remain to be elucidated. Methods: We established a C57BL/6 mouse model of chronic migraine (CM) using recurrent intraperitoneal injections of nitroglycerin (NTG, 10 mg/kg), and prophylactic treatment was simulated by administering NBP (30 mg/kg, 60 mg/kg, 120 mg/kg) by gavage prior to each NTG injection. Mechanical threshold was assessed using von Frey fibers, and photophobia and anxious behaviours were assessed using a light/dark box and elevated plus maze. Expression of c-Fos, calcitonin gene-related peptide (CGRP), Nucleus factor erythroid 2-related factor 2 (Nrf2) and related pathway proteins in the spinal trigeminal nucleus caudalis (SP5C) were detected by Western blotting (WB) or immunofluorescence (IF). The expression of IL-1β, IL-6, TNF-α, Superoxide dismutase (SOD) and malondialdehyde (MDA) in SP5C and CGRP in plasma were detected by ELISA. A reactive oxygen species (ROS) probe was used to detect the expression of ROS in the SP5C. Results: At the end of the modelling period, chronic migraine mice showed significantly reduced mechanical nociceptive thresholds, as well as photophobic and anxious behaviours. Pretreatment with NBP attenuated nociceptive sensitization, photophobia, and anxiety in the model mice, reduced expression levels of c-Fos and CGRP in the SP5C and activated Nrf2 and its downstream proteins HO-1 and NQO-1. By measuring the associated cytokines, we also found that NBP reduced levels of oxidative stress and inflammation. Most importantly, the therapeutic effect of NBP was significantly reduced after the administration of ML385 to inhibit Nrf2. Conclusions: Our data suggest that NBP may alleviate migraine by activating the Nrf2 pathway to reduce oxidative stress and inflammation in migraine mouse models, confirming that it may be a potential drug for the treatment of migraine. [ABSTRACT FROM AUTHOR]

Phthalates (PAEs), a group of environmental endocrine disruptors, are associated with oxidative stress and have adverse effects on female ovarian reserves. However, this association has been poorly investigated, particularly with respect to clinical evidence. In this study, we provided clinical evidence of a relationship between exposure levels of PAEs, oxidative stress and decreased ovarian reserve (DOR). Firstly, the urinary concentrations of metabolites of PAEs were measured by high performance liquid chromatography coupled with tandem mass spectrometry (HPLC-MS/MS). The serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and anti-Mullerian hormone (AMH), and the biomarkers of oxidative stress, malondialdehyde (MDA), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC), were determined. Finally, statistical analyses were conducted to describe the relationship between the PAEs exposure, oxidative stress and DOR. We found that the levels of monomethyl phthalate (MMP), monoisobutyl phthalate (MiBP), mono-(2-ethylhexyl) phthalate (MEHP), and mono-(2-ethyl-5-hydroxypentyl) phthalate (MECPP) in the DOR group were significantly higher than those in the control group. There was a significant negative association between AMH and MMP, MiBP levels. and a significant positive association between FSH and MMP levels. PAEs exposure was also associated with a significant increase in MDA levels and decrease in SOD levels. In conclusion, the exposure of PAEs was closely associated with DOR, potentially mediated by oxidative stress pathways; however, small sample size was a limitation in this study. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus, a condition preceded by prediabetes, is documented to compromise skeletal muscle health, consequently affecting skeletal muscle structure, strength, and glucose homeostasis. A disturbance in skeletal muscle functional capacity has been demonstrated to induce insulin resistance and hyperglycemia. However, the modifications in skeletal muscle function in the prediabetic state are not well elucidated. Hence, this study investigated the effects of diet-induced prediabetes on skeletal muscle strength in a prediabetic model. Male Sprague Dawley rats were randomly assigned to one of the two groups (n = 6 per group; six prediabetic (PD) and six non-pre-diabetic (NPD)). The PD group (n = 6) was induced with prediabetes for 20 weeks. The diet that was used to induce prediabetes consisted of fats (30% Kcal/g), proteins (15% Kcal/g), and carbohydrates (55% Kcal/g). In addition to the diet, the experimental animals (n = 6) were supplied with drinking water that was supplemented with 15% fructose. The control group (n = 6) was allowed access to normal rat chow, consisting of 35% carbohydrates, 30% protein, 15% fats, and 20% other components, as well as ordinary tap water. At the end of week 20, the experimental animals were diagnosed with prediabetes using the American Diabetes Association (ADA) prediabetes impaired fasting blood glucose criteria (5.6–6.9 mmol/L). Upon prediabetes diagnosis, the animals were subjected to a four-limb grip strength test to assess skeletal muscle strength at week 20. After the grip strength test was conducted, the animals were euthanized for blood and tissue collection to analyze glycated hemoglobin (HbA1c), plasma insulin, and insulin resistance using the homeostatic model of insulin resistance (HOMA-IR) index and malondialdehyde (MDA) concentration. Correlation analysis was performed to examine the associations of skeletal muscle strength with HOMA-IR, plasma glucose, HbA1c, and MDA concentration. The results demonstrated increased HbA1c, FBG, insulin, HOMA-IR, and MDA concentrations in the PD group compared to the NPD group. Grip strength was reduced in the PD group compared to the NPD group. Grip strength was negatively correlated with HbA1c, plasma glucose, HOMA-IR, and MDA concentration in the PD group. These observations suggest that diet-induced prediabetes compromises muscle function, which may contribute to increased levels of sedentary behavior during prediabetes progression, and this may contribute to the development of hyperglycemia in T2DM. [ABSTRACT FROM AUTHOR]

A systematic theoretical study was conducted on the triel bonds (TrB) within the BH3∙∙∙M(MDA)2 and C5H4BX∙∙∙M(MDA)2 (M = Ni, Pd, Pt, X = H, CN, F, CH3, NH2, MDA = enolated malondialdehyde) complexes, with BH3 and C5H4BX acting as the electron acceptors and the square-coordinated M(MDA)2 acting as the electron donor. The interaction energies of these systems range between −4.71 and −33.18 kcal/mol. The larger the transition metal center M, the greater the enhancement of the TrB, with σ–hole TrBs found to be stronger than π–hole TrBs. In the σ–hole TrB complex, an electron-withdrawing substituent on the C opposite to the B atom enhances the TrB, while an electron-donating substituent has little effect on the strength of TrB in the Pd and Pt complexes but enhances the TrB in the Ni-containing complexes. The van der Waals interaction plays an important role in stabilizing these binary systems, and its contribution diminishes with increasing M size. The orbital effect within these systems is largely due to charge transfer from the dz2 orbital of M into the empty pz orbital of B. [ABSTRACT FROM AUTHOR]

Purpose: Varicoceles can be a source of elevated seminal oxidative stress (OS) and sperm DNA fragmentation (SDF). However, it remains unclear whether varicocele repair (VR) could reduce these parameters. This systematic review and meta-analysis (SRMA) aims to investigate the impact of VR on SDF and seminal malondialdehyde (MDA). Materials and Methods: A literature search was performed in Scopus, PubMed, Ovid, Embase, and Cochrane databases. This SRMA included randomized controlled trials and observational studies reporting the pre- and postoperative levels of SDF and seminal OS in infertile men with clinical varicocele that underwent VR. Subgroup analyses included techniques of VR and SDF testing. The effect size was expressed as standardized mean difference (SMD). Results: Out of 1,632 abstracts assessed for eligibility, 29 studies with 1,491 infertile men were included. The analysis showed a significant reduction in SDF after VR, compared to preoperative values (SMD –1.125, 95% confidence interval [CI] –1.410, –0.840; p<0.0001) with high inter-study heterogeneity (I2 =90.965%). Reduction in SDF was evident with microsurgical technique and non-microsurgical inguinal approaches (SMD –1.014, 95% CI –1.263, –0.765; p<0.0001, and SMD –1.495, 95% CI –2.116, –0.873; p<0.0001), respectively. Reduction in SDF was significant irrespective of testing was done by sperm chromatin dispersion (SMD –2.197, 95% CI –3.187, –1.207; p<0.0001), sperm chromatin structure assay (SMD –0.857, 95% CI –1.156, –0.559; p<0.0001) or TUNEL (SMD –1.599, 95% CI –2.478, –0.719; p<0.0001). A significant decrease in seminal MDA levels was observed following VR (SMD –2.450, 95% CI –3.903 to –0.997, p=0.001) with high inter-study heterogeneity (I2 =93.7%). Conclusions: Using pre- and post-intervention data, this SRMA indicates a significant reduction in SDF and seminal MDA levels in infertile men with clinical varicocele treated with VR. These findings may have important implications for the future management of this selected group of infertile patients. [ABSTRACT FROM AUTHOR]

Background Depression is one of the most common psychological disorders that can affect a person’s mood and change his/her perception of the self and environment. Melilotus officinalis L. plant contains effective substances and antioxidant compounds. Objective The present study aims to investigate the antidepressant effects of alcoholic extract of Melilotus officinalis L. in male rats. Methods In this experimental research, 42 male rats were divided into six groups of 7 including control (normal saline), negative control (reserpine), positive control (reserpine+fluoxetine) and three reserpine groups treated by intraperitoneal injection of 100, 200, 400 mg/kg doses of alcoholic extract of Melilotus officinalis L. Behavioral tests including forced swim test (FST) and tail suspension test (TST) were used to evaluate depression, and the antioxidant capacity and malondialdehyde level were also measured. The data were analyzed in SPSS software, version 20 using one-way analysis of variance. The significance level was set at P<0.05. Results The 200 mg/kg and 400 mg/kg doses of alcoholic extract significantly reduced the duration of immobility in the FST compared to the negative control. In the TST, the doses of 200 and 400 mg/kg showed a significant increase compared to the negative control. The doses of 200 and 400 mg/kg significantly increased the antioxidant capacity of the brain compared to the negative control. The doses of 200 and 400 mg/kg significantly reduced the antioxidant capacity of the brain compared to the negative control. Conclusion The alcoholic extract of Melilotus officinalis L has antidepressant effects similar to fluoxetine probably due to its antioxidant compounds. [ABSTRACT FROM AUTHOR]

INTRODUCTION This study aimed to investigate the effects of nicotine on the activation of pancreatic stellate cells (PSCs) and pancreatic fibrosis in chronic pancreatitis (CP), along with its underlying molecular mechanisms. METHODS This was an in vivo and in vitro study. In vitro, PSCs were cultured to study the effects of nicotine on their activation and oxidative stress. Transcriptome sequencing was performed to identify potential signaling pathways involved in nicotine action. And the impact of nicotine on mitochondrial Ca2+ levels and Ca2+ transport-related proteins in PSCs was analyzed. The changes in nicotine effects were observed after the knockdown of the mitochondrial calcium uniporter (MCU) in PSCs. In vivo experiments were conducted using a mouse model of CP to assess the effects of nicotine on pancreatic fibrosis and oxidative stress in mice. The alterations in nicotine effects were observed after treatment with the MCU inhibitor Ru360. RESULTS In vitro experiments demonstrated that nicotine promoted PSCs activation, characterized by increased cell proliferation, elevated α-SMA and collagen expression. Nicotine also increased the production of reactive oxygen species (ROS) and cellular malondialdehyde (MDA), exacerbating oxidative stress damage. Transcriptome sequencing revealed that nicotine may exert its effects through the calcium signaling pathway, and it was verified that nicotine elevated mitochondrial Ca2+ levels and upregulated MCU expression. Knockdown of MCU reversed the effects of nicotine on mitochondrial calcium homeostasis, improved mitochondrial oxidative stress damage and structural dysfunction, thereby alleviating the activation of PSCs. In vivo validation experiments showed that nicotine significantly aggravated pancreatic fibrosis in CP mice, promoted PSCs activation, exacerbated pancreatic tissue oxidative stress, and increased MCU expression. However, treatment with Ru360 significantly mitigated these effects. CONCLUSIONS This study confirms that nicotine upregulates the expression of MCU, leading to mitochondrial calcium overload and exacerbating oxidative stress in PSCs, and ultimately promoting PSCs activation and exacerbating pancreatic fibrosis in CP. [ABSTRACT FROM AUTHOR]

Our current study examines the significant impact of aniline on the fish feed freshwater benthic annelid, Tubifex tubifex, including mortality, changes in total protein concentration and antioxidant enzyme activity (catalase, superoxide dismutase, glutathione-s transferase and glutathione peroxidase), as well as the generation of oxidative stress (by assessing malondialdehyde concentration). The 96-hour LC50 value of aniline is 276.940 mg/L. The General Unified Threshold Model of Survival (GUTS) was used to validate the survival rate pattern of the test organism in response to aniline at the acute level, with the GUTS-SD model better correctly predicting the expected course of population death. During long-term bioassay antioxidant enzymes activities (superoxide dismutase, glutathione-s transferase and glutathione peroxidase) and oxidative stress biomarkers concentration (malondialdehyde concentration) is substantially enhanced while protein concentration and Catalase activity are markedly reduced during the bioassay. The stress and detrimental effects of aniline on Tubifex tubifex were examined in the current study, taking into account all biomarkers, by utilising the Integrated Biomarker Response index. The results show that exposure to toxicants like aniline has a detrimental effect on Tubifex tubifex's survival rate and general health. [ABSTRACT FROM AUTHOR]

Background: Cell phone and Ultra-High Frequency (UHF) waves produce oxidative stress and cause testicular toxicity. This investigation was directed to evaluate the effectiveness of Rosmarinic Acid (RA) against oxidative stress caused by UHF radiation in rats. Methods: Forty-two male Wistar rats were divided into six groups. The control received 5 mL normal saline (0.9% NaCl) by gavage, the cell phone group received 915 MHz, the UHF waves group just received 2450 MHz, the RA/cell phone group received RA plus 915 MHz, RA/UHF waves group received RA plus 2450 MHz, and RA just received RA (20 mg/kg). After 30 days of consecutive radiation, the biochemical and histopathological parameters of their testes were measured. Statistical comparison was made using one-way ANOVA followed by Tukey's post hoc test. Results: Cell phone and UHF wave radiation significantly diminished the activity of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase, and glutathione content (P<0.001). On the opposite, UHF significantly increased oxidative stress indices including malondialdehyde level, nitric oxide level, and protein carbonyl content (P<0.001). UHF also significantly reduced the number of Sertoli cells, spermatogonia, primary spermatocyte, epithelial height, and seminiferous tubular and luminal diameters (P<0.001). RA, as an effective antioxidant, reverses the above-mentioned harms and moderates the adverse effects of UHF on the testes of rats by significantly diminishing the oxidative stress indices and antioxidant enzyme rise and improving the histological parameters (P<0.001). Conclusion: RA can protect the testes of rats from UHF- induced toxicity by reducing oxidative stress. RA as a food supplement might be useful for protecting humans exposed to UHF environmental contamination. [ABSTRACT FROM AUTHOR]

The radiolysis of malondialdehyde (MDA) in acidic (pH 3) and alkaline (pH 11) aqueous solutions has been studied using UV spectrometry, HPLC, and chemical analysis. It has been found that in an acidic medium, the radiation-chemical yield of degradation of MDA at concentrations greater than 3 × 10–4 mol/L exceeds 10 molecule/100 eV, indicating the occurrence of chain processes. It has been established that dissolved oxygen plays an important role in the chain process of MDA decomposition. A system of reactions was proposed to explain the results of the experiments. [ABSTRACT FROM AUTHOR]

The broadband UV photochemistry kinetics of acetylacetaldehyde, the hybrid form between malonaldehyde and acetylacetone (the two other most simple molecules exhibiting an intramolecular proton transfer), trapped in four cryogenic matrices, neon, nitrogen, argon, and xenon, has been followed by FTIR and UV spectroscopy. After deposition, only the two chelated forms are observed while they isomerize upon UV irradiation toward nonchelated species. From previous UV irradiation effects, we have already identified several nonchelated isomers, capable, in turn, of isomerizing and fragmenting; even fragmentation seems to be most unlikely due to cryogenic cages confinement. Based on these findings, we have attempted an approach to understand the reaction path of electronic relaxation. Indeed, we have demonstrated, in previous studies, that in the case of malonaldehyde, this electronic relaxation pathway proceeds through singlet states while it proceeds through triplet ones in the case of acetylacetone. We observed CO and CO2 formations when photochemistry is almost observed among nonchelated forms, i.e., when the parent molecule is almost totally consumed. In order to identify a triplet state transition, we have tried to observe a "heavy atom effect" by increasing the weight of the matrix gas, from Ne to Xe, and to quench the T1 state by doping the matrices with O2. It appears that, as in the case of acetylacetone, it is the nonchelated forms that fragment. It also appears that these fragmentations certainly take place in the T1 triplet state and originate in an Π* ← n transition. [ABSTRACT FROM AUTHOR]

It has been shown that the transport of electrons in the respiratory chain of mitochondria, ion-transport processes, the balance of Ca2+ ions and other metabolic processes in the cell are intrinsically connected with lipoperoxidation processes. In particular, in recent years, plant biologically active compounds have been widely used to eliminate oxidative processes developing in the body. Accordingly, we considered it important to study the mechanisms of action of xylopyr-T, glucopyr-T and 2-DVG polyphenols isolated from the plants Plantago major L. and Plantago lanceolata L., belonging to the Plantaginaceae family, which are widely used in folk medicine. Therefore, in vitro experiments, the amount of malondialdehyde and the condition state of mPTP were studied by spectrophotometric method. The obtained results revealed that the studied polyphenols inhibit lipoperoxidation induced by Fe2+/ascorbate the production of malondialdehyde was reduce by xylopyr-T to 81.9 ± 1.2 %, by glucopyr-T to 79.4 ± 1.7 % and by 2-DVG to 75.0 ± 1.8 % at a concentration of 4 μM in rat liver mitochondria. At the same time, mPTP opening in the medium with the substrate succinate (+ rotenone) inhibition 2-DVG polyphenol at a concentration of 100 μM was reduced by 84.5 ± 2.8 %, xylopyr-T polyphenol at a concentration of 200 μM by 67.6 ± 4.8 % and it was shown that glucopyr-T polyphenol at a concentration of 200 μM by 32.5 ± 1.65 % compared to the control. In conclusion, it can be illustrated that the studied polyphenols, along with their high antioxidant properties, show a structure-dependent inhibition of mPTP opening, which is involved in various physiological and pathological processes. [ABSTRACT FROM AUTHOR]

Background: Preterm birth (PTB) poses a significant global health challenge and focused research is vital for improving maternal and neonatal health outcomes. The purpose of this study was to determine the effect of oxidative stress (OS) and DNA damage on PTB. Methods: There were two groups: (a) cases consisting of mothers with PTB (<37 weeks of gestation, n = 100) and (b) controls consisting of mothers with term birth (>37 weeks of gestation, n = 100). Women with vaginal infection, non-cephalic presentation, multiple gestations, fetal anomalies, Cesarean delivery, pregnancy with Mullerian anomalies, or preeclampsia were excluded from the study. OS analysis was conducted by measuring levels of superoxide dismutase (SOD), catalase (CAT), lipid peroxidation (LPO), and total protein and DNA damage were evaluated by CBMN-Cyt assay. Statistical analysis was performed using students' t -test and one-way ANOVA. Results: Low levels of antioxidants SOD and CAT (p <.0001), and total protein (p <.0001), besides high malondialdehyde (byproduct of LPO) (p <.0001) were observed in the PTB group. Moreover, high frequencies of micronuclei (p <.0001) and nucleoplasmic buds (p <.01) were detected in the PTB mothers compared to term birth mothers, while no significance was observed in the nucleoplasmic bridge frequencies. Conclusion: When the body's immune system and antioxidants fail to cope up with the generated OS, it can lead to PTB. Along with other body tests, OS markers and CBMN-Cyt tests have the potential to be used in diagnostics for early warning as well as monitoring and advising mothers for a better pregnancy outcome. [ABSTRACT FROM AUTHOR]

The present study was conducted to investigate the effects of Ocimum basilicum L. (OB) extract on learning and memory impairment in aged rats. Male rats were divided into the following experimental groups: Group 1 (control): including 2 months old rats, Group 2 (aged) including 2 years old rats, Groups 3–5 (aged-OB): including 2 years old rats received 50, 100, and 150 mg/kg OB for 8 weeks by oral gavage. Aging increased the delay to find the platform but, however, decreased the time spent in the target quadrant when tested by Morris water maze (MWM). Aging also reduced the latency to enter the dark chamber in the passive avoidance (PA) test compared to the control group. Moreover, interleukin-6 (IL-6) and malondialdehyde (MDA) levels were raised in the hippocampus and cortex of aged rats. In contrast, thiol levels and enzymatic activity of superoxide dismutase (SOD) and catalase (CAT) significantly reduced. In addition, aging significantly reduced BDNF expression. Finally, OB administration reversed the mentioned effects. The current research showed that OB administration improves learning/memory impairment induced by aging. It also found that this plant extract protects the brain tissues from oxidative damage and neuroinflammation. [ABSTRACT FROM AUTHOR]

Background: Ferroptosis is known to play a crucial role in diabetic osteopathy. However, key genes and molecular mechanisms remain largely unclear. This study aimed to identify a crucial ferroptosis-related differentially expressed gene (FR-DEG) in diabetic osteopathy and investigate its potential mechanism. Methods: We identified fibronectin type III domain-containing protein 5 (FNDC5)/irisin as an essential FR-DEG in diabetic osteopathy using the Ferroptosis Database (FerrDb) and GSE189112 dataset. Initially, a diabetic mouse model was induced by intraperitoneal injection of streptozotocin (STZ), followed by intraperitoneal injection of irisin. MC3T3-E1 cells treated with high glucose (HG) were used as an in vitro model. FNDC5 overexpression plasmid was used to explore underlying mechanisms in vitro experiments. Femurs were collected for micro-CT scan, histomorphometry, and immunohistochemical analysis. Peripheral serum was collected for ELISA analysis. Cell viability was assessed using a CCK-8 kit. The levels of glutathione (GSH), malondialdehyde (MDA), iron, reactive oxygen species (ROS), and lipid ROS were detected by the corresponding kits. Mitochondria ultrastructure was observed through transmission electron microscopy (TEM). Finally, mRNA and protein expressions were examined by quantitative real‐time PCR (qRT‐PCR) and western blot analysis. Results: The expression of FNDC5 was found to be significantly decreased in both in vivo and in vitro models. Treatment with irisin significantly suppressed ferroptosis and improved bone loss. This was demonstrated by reduced lipid peroxidation and iron overload, increased antioxidant capability, as well as the inhibition of the ferroptosis pathway in bone tissues. Furthermore, in vitro studies demonstrated that FNDC5 overexpression significantly improved HG-induced ferroptosis and promoted osteogenesis. Mechanistic investigations revealed that FNDC5 overexpression mitigated ferroptosis in osteoblasts by inhibiting the eukaryotic initiation factor 2 alpha (eIF2α)/activated transcription factor 4 (ATF4)/C/EBP-homologous protein (CHOP) pathway. Conclusions: Collectively, our study uncovered the important role of FNDC5/irisin in regulating ferroptosis of diabetic osteopathy, which might be a potential therapeutic target. [ABSTRACT FROM AUTHOR]

Background: Plants are considered the primary source of many principal bioactive compounds that have been utilized in a wide range of applications including the pharmaceutical and biotechnological industries. Therefore, there is an imperative need to modulate the production of natural bioactive components. The present study aimed to determine the importance of dried and pulverized date palm seeds (DPS) as a natural elicitor for the synthesis of secondary metabolites in Lotus arabicus L. Results: The presence of various antioxidant compounds, simple sugars, amino acids, fatty acids and reasonable mineral contents was distinct in the phytochemical characterization of DPS. The major components detected in DPS analysis were the 5-(hydroxymethyl) furfural and 2,3-dihydro-3,5-dihydroxy-6-methyl-4H-pyranone. The induced callus of L. arabicus (seven weeks old) was supplemented with DPS at different concentrations (0, 2, 4, 8 and 10 g/l) in culture media. Treatment with 8 g/l DPS induced the highest antioxidant capacity, ascorbic acid content and secondary metabolites (total phenolics and flavonoids) in the produced callus. Stress biomarkers (hydrogen peroxide and malondialdehyde) were found in the control ranges except at 10 g/l DPS. The expression patterns of key genes involoved in secondary metabolism modulation, such as phenylalanine ammonia lyase (PAL), chalcone synthase (CHS), chalcone isomerase (CHI), flavonol synthase (FLS) and deoxyxylulose phosphate reductoisomerase (DXR), were triggered after DPS treatments. Moreover, the quantitative profiling of phenolic and flavonoid compounds showed that supplementation with DPS, especially at 8 g/l, led to pronounced increases in most of the measured compounds. Conclusion: The marked upregulation of eliciting-responsive genes and overproduction of secondary metabolites provide molecular-based evidence for intensifying the principal pathways of phenylpropanoid, flavonoid and terpenoid biosynthesis. Overall, the present in vitro study highlights the stimulating capacity of DPS utilization to improve the bioactive components of L. arabicus at the physiological and molecular levels, enhancing its potential as a medicinal herb. [ABSTRACT FROM AUTHOR]

Background: Ferroptosis, a non-apoptotic form of cell death induced by accumulation of free iron ions and lipid peroxidation, its importance for cancer treatment is gradually being recognized. Research on the anti-cancer mechanism of juglone is accumulating. However, the specific mechanism by which it directs glioblastoma (GBM) to death is unknown. Methods: We used in vitro and in vivo experiments to explore the anti-GBM effect generated by juglone through the ferroptosis pathway. Results: Juglone mainly causes cell death by inducing ferroptosis. Mechanistically, juglone can significantly activate the phosphorylation of p38MAPK. According to transcriptome sequencing and protein interaction analysis, the Nrf2-GPX4 signaling pathway is identified as the primary pathway through which juglone mediates ferroptosis. In vitro and in vivo experiments further verified that juglone induces the ferroptosis of GBM by activating the phosphorylation of p38MAPK and negatively regulating the Nrf2-GPX4 signaling pathway. Conclusion: Juglone induces ferroptosis and inhibits the growth of GBM by targeting the Nrf2/Gpx4 signaling pathway and thus holds promise as a novel ferroptosis inducer or anti-GBM drug. [ABSTRACT FROM AUTHOR]

Background. Diabetes mellitus (DM) presents a significant global health challenge with considerable cardiovascular implications. Coenzyme Q10 (CoQ10) has gained recognition for its potential as a natural antioxidant supplement in the management of diabetes and its associated cardiovascular complications. Aim. This comprehensive review systematically examines the scientific rationale underlying the therapeutic properties of CoQ10 in mitigating the impact of diabetes and its cardiovascular consequences. The analysis encompasses preclinical trials (in vitro and in vivo) and clinical studies evaluating the efficacy and mechanisms of action of CoQ10. Result & Discussion. Findings reveal that CoQ10, through its potent antioxidant and anti-inflammatory attributes, demonstrates significant potential in reducing oxidative stress, ameliorating lipid profiles, and regulating blood pressure, which are crucial aspects in managing diabetes-induced cardiovascular complications. CoQ10, chemically represented as C59H90O4, was administered in capsule form for human studies at doses of 50, 100, 150, 200, and 300 mg per day and at concentrations of 10 and 20 μM in sterile powder for experimental investigations and 10 mg/kg in powder for mouse studies, according to the published research. Clinical trials corroborate these preclinical findings, demonstrating improved glycemic control, lipid profiles, and blood pressure in patients supplemented with CoQ10. Conclusion. In conclusion, CoQ10 emerges as a promising natural therapeutic intervention for the comprehensive management of diabetes and its associated cardiovascular complications. Its multifaceted impacts on the Nrf2/Keap1/ARE pathway, oxidative stress, and metabolic regulation highlight its potential as an adjunct in the treatment of diabetes and related cardiovascular disorders. However, further extensive clinical investigations are necessary to fully establish its therapeutic potential and assess potential synergistic effects with other compounds. [ABSTRACT FROM AUTHOR]

A particular attribute of the brain lies in the ability to learn, acquire information from the environment, and utilize the learned information. Previous research has noted that various factors (e.g., age, stress, anxiety, pathological issues), including antipsychotic medications, affect the brain and memory. The current study aimed to reveal the effects of chronic metformin treatment on the cognitive performance of rats and on commonly measured markers for oxidative stress. Wistar male rats (n = 40) were randomly divided into four groups: CTR (n = 10)–control group, METF (n = 10)–animals receiving metformin 500 mg/kg, HAL (n = 10)–animals receiving haloperidol 2 mg/kg, and HALMETF (n = 10)–animals receiving haloperidol 2 mg/kg and metformin 500 mg/kg. The medication was administered daily by oral gavage for 40 days. Memory and learning were assessed using the Morris Water Maze (MWM) test. At the end of the MWM, the rodents were decapitated under anesthesia, and the brain and blood samples were assayed by liquid chromatography for markers of oxidative stress (malondialdehyde, MDA, reduced/oxidized glutathione ratio, GSH/GSSG). The quantification of brain-derived neurotrophic factor (BDNF) was performed using the conventional sandwich ELISA technique. In the HALMETF group, metformin attenuated the negative effects of haloperidol. Brain and plasma MDA levels increased in the HAL group. Brain and plasma GSH/GSSG ratios and BDNF levels did not reveal any differences between groups. In conclusion, metformin treatment limits the deleterious cognitive effects of haloperidol. The effect on oxidative stress markers may also point toward an antioxidant-like effect of metformin, but this needs further tests for confirmation. [ABSTRACT FROM AUTHOR]

The research includes studying the levels of hydrogen sulphide (H2S) and cystathionine γ-lyase (CSE) with some oxidants and antioxidants in the serum of patients with epilepsy disease in Mosul city which include: malondialdehyde (MDA), peroxynitrite (ONOO-), glutathione (GSH), total bilirubin (TSB), albumin (Alb) and uric acid (UA), were measured in the patient group who suffered from epilepsy disease in Mosul city, Samples reached (116), which included: (56) samples for epilepsy patients group, and (60) for control group. The results showed there was a significant decrease in the levels of H2S, CSE, GSH, and TSB and a significant increase in the levels of MDA, ONOO-, Alb and UA in serum for epilepsy patients when Compared with the control group. The study concluded that H2S gas produced within the body and CSE suffer from low levels within the body, and they also decrease with the increase in the duration of the disease as a result of their use as protective functions in the body against epilepsy disease and developing it, by observing the levels of oxidants and antioxidants compounds and stimulating the body to increase their levels (H2S, and CSE) in various ways can lead to improving the health condition of patients. [ABSTRACT FROM AUTHOR]

Arsenic (As) is a metal with potentially toxic effects on different organisms. Hydrogen sulfide (H2S) plays a vital role in mitigating heavy metal toxicity by reducing oxidative stress in plants and animals. However, the role of H2S in alleviating arsenic toxicity in yeast cells remains unclear. In this study, the role of NaHS (exogenous physiological H2S) in alleviating As-induced yeast cell death was investigated. Yeast cells in the logarithmic phase were pretreated with 0.05 mmol/L NaHS for 6 h, and then incubated in the YPD medium with or without 1 mmol/L As. After 12 h of treatment, relative survival rate, H2S content, oxidative stress biomarkers, and antioxidant machinery were measured. Our results showed that sodium arsenite-induced yeast cell death and pretreatment with 0.05 mmol/L NaHS significantly alleviated sodium arsenite-induced cell death. Under sodium arsenite conditions, the levels of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) increased, accompanied by the inhibition of the catalase (CAT) activity and the downregulation of CTT1 expression. However, the activities of the superoxide dismutase (SOD) and glutathion peroxidase (GPX) increased, and the expression of SOD1 and GPX2 was markedly upregulated in the group treated with sodium arsenite. When yeast cells were pretreated with NaHS, the intracellular ROS and MDA levels decreased significantly, and the activities of SOD, CAT, and GPX increased significantly. This was associated with a significant increase in relative survival rate and H2S content compared to the arsenic treatment alone. Our findings indicate that NaHS alleviates sodium arsenite-induced yeast cell death, mainly by enhancing the antioxidant defense system. [ABSTRACT FROM AUTHOR]

OBJECTIVE: In this study, the effect of tocilizumab (TCZ) on lung tissue in lung ischemia-reperfusion (I/R) injury in rats was investigated. MATERIAL AND METHODS: A total of 24 Wistar rats were divided into 4 equal groups, with 6 rats in each group: Left lung I/R was applied to I/R groups. In the I/R groups, the left lung hilum was clamped for 45 minutes, and then the clamp was removed and reperfused for 120 minutes. In the TCZ groups, 4 mg/kg and 8 mg/kg of TCZ were administered intraperitoneally to the rats 30 minutes before surgery. RESULTS: The tumor necrosis factor-alpha mean value was not statistically significant between the groups (P = .091). Statistically significant results were observed between group I/R-TCZ (8 mg/kg) and group I/R for catalase. (P = .005). Statistically significant results were observed between group I/R-TCZ (8 mg/kg) and group I/R for malondialdehyde. (P = .009). The difference in total ischemia score between group I/R-TCZ (4 mg/kg) and group I/R-TCZ (8 mg/kg) and group I/R was statistically significant (P < .001). In terms of alveolar hemorrhage, there was a statistically significant difference between group I/R-TCZ (4 mg/kg) and group I/R-TCZ (8 mg/kg) and group I/R (P = .01 and P = .002, respectively). There was a statistically significant difference between group I/R-TCZ (8 mg/kg) and group I/R in terms of neutrophil accumulation (P = .01). In terms of interstitial edema, there was a statistically significant difference between group I/R-TCZ (4 mg/kg) and group I/R-TCZ (8 mg/kg) and group I/R (P = .006 and P = .001, respectively). In terms of pulmonary edema, there was a statistically significant difference between group I/R-TCZ (4 mg/kg) and group I/R-TCZ (8 mg/kg) and group I/R (P = .01 and P = .009, respectively). CONCLUSION: Lung tissue may be affected by I/R injury and this damage can be reversed with the use of TCZ. [ABSTRACT FROM AUTHOR]

Advanced glycation end products (AGEs) are a large number of heterogeneous compounds formed by the glycation of proteins, fats or nucleic acids. Endogenous AGEs have been associated with various health problems such as obesity, type 2 diabetes mellitus and cardiovascular disease. Inflammation is thought to be one of the main mechanisms in the development of these disorders. Although AGEs are produced endogenously in the body, exogenous sources such as smoking and diet also contribute to the body pool. Therefore, when the AGE pool in the body rises above physiological levels, different pathological conditions may occur through various mechanisms, especially inflammation. While the effects of endogenous AGEs on the development of inflammation have been studied relatively extensively, and current evidence indicates that dietary AGEs (dAGEs) contribute to the body's AGE pool, it is not yet known whether dAGEs have the same effect on the development of inflammation as endogenous AGEs. Therefore, this review aimed to evaluate the results of cross‐sectional and intervention studies to understand whether dAGEs are associated with inflammation and, if there is an effect on inflammation, through which mechanisms this effect might occur. [ABSTRACT FROM AUTHOR]

The herb Hylocereus undatus, which is rich in phytochemicals and thought to contain antioxidants comparable to those in its peel, has a lot of promise for use in the food field. The presented study aimed to study the protective effect of the aqueous extrac and the active compounds (gallic acid) isolated from the dragon fruit (H. undates) to lessen the impact of rheumatoid arthritis (RA) induced by Freund's Complete Adjuvant (CFA)) by studying some of the changes in biochemical and histochemical parameters. The Wistar albino rats (male) were divided into four groups viz., Group I: A negative control group, dosed only with plain water orally, Group II: Induced for RA by CFA, a positive control group; Group III: dosed with aqueous extract of the fruit of H. undatus (kg/500 mg); and Group IV: dosed with gallic acid isolated from this fruit (kg/mg20). The results showed a significant increase in malondialdehyde (MDA), platelet, interleukin 6 (IL-6), and RF in rats treated with CFA and a significant decrease in Hb compared to the negative control group. There was a significant decrease of MDA, Platelet, IL-6, and RF in the groups treated with aqueous extract and a significant increase in Hb compared with the positive control group while there was a significant decrease in each of MDA, platelets, IL-6, and RF. Based on a histological analysis, the study group's liver and kidneys had smaller lesions and different abnormalities than the control. Thus, the fruit plant's gallic acid extracts were protective in reducing RA damage caused by CFA and improving kidney and liver tissue. [ABSTRACT FROM AUTHOR]