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Copyright of Gümüshane Üniversitesi Saglik Bilimleri Dergisi is the property of Gumushane University, Faculty of Health Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Sepsis is a systemic infectious disease that leads to shock, organ failure, and death and requires urgent treatment. Animal model studies of sepsis and endotoxemia have revealed that antioxidant compounds prevent the progression of multi-system organ failure and reduce death rate. In the present study aimed to establish the effect of propolis, which has been proven to have antibacterial, anti-inflammatory and antioxidant activities in recent years, on lipopolysaccharide (LPS)-induced renal damage. 40 Sprague dawley rats were randomly divided into five equal groups (n = 8): Control (0.9% NaCl), LPS (30 mg/kg), propolis (250 mg/kg), propolis + LPS, and LPS + propolis. After completion of the experimental protocol, Malondialdehyde (MDA) levels were measured using blood serum samples obtained from the rats. The kidney samples of the rats were examined histopathologically. As a result, it was determined that LPS increased MDA levels in the blood serum samples and it caused histological changes in the kidney tissue such as tubular damage, mild ischemic injury, ischemic damage in the form of vacuolization, tubular epithelial vacuolization, vascular congestion, and glomerular atrophy. Contrary to these results, MDA levels of serum decreased in the propolis + LPS, and LPS + propolis groups, and also histological findings improved. These results showed that protective effect of propolis against kidney damage caused by LPS.

Tamoxifen (TAM) is an antiestrogenic agent used for adjuvant treatment in estrogen receptor‐positive breast cancers in the pre/post‐menopausal period. This study, it was aimed to determine the effect of olive oil extract of propolis (OEP) on short and long‐term administration of TAM in rats. Wistar albino rats were divided into groups with eight animals in each. Groups: control, OEP, TAM, and OEP + TAM. At the end of the experiment, oxidative stress tests were performed with Enzyme‐Linked ImmunoSorbent Assay (ELISA) on blood and tissue samples (liver, kidney, and ovary) taken from rats. After single‐dose TAM administration, there was a significant increase in red blood cell, hematocrit, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration levels compared to the control group, a decrease in low‐density lipoprotein (LDL) value, a significant increase in liver enzymes and fasting glucose values was detected compared with the control and propolis groups. A normalizing effect was observed in the group given OEP and TAM combined. The increase in Malondialdehyde (MDA) and the decrease in enzyme activities in tissues are also noteworthy. Propolis application reduced the tissue damage caused by TAM. In addition, improved cytokine levels, which increased with TAM administration. It has been concluded that OEP can be given in supportive treatment, as it improves hematological and antioxidant parameters in TAM treatment. [ABSTRACT FROM AUTHOR]

Type 1 diabetes mellitus (T1DM) is one of the main causes of ovarian atresia, but its molecular effect on the ovaries is not fully understood. Accumulating evidence suggests that T1DM causes excessive endoplasmic reticulum (ER) stress and insufficient adaptive unfolded protein response that triggers proapoptotic signaling pathways in ovarian tissue. In addition, problems such as amenorrhea and infertility, which are frequently seen in women with T1DM, continue despite the intensification of insulin therapy and improvement of metabolic control. Therefore new, and adjunctive treatments for women with T1DM need to be explored. We aimed to examine how the use of linagliptin, which has blood sugar‐lowering effects and high antioxidant activity, together with insulin affects the expression levels of proteins and genes that play a role in ER stress in type 1 diabetic mouse ovaries. Eighty‐four Balb/C 6‐week‐old female mice were randomly divided into seven groups: control, vehicle, diabetes + insulin, diabetes + linagliptin, diabetes + linagliptin + insulin, diabetes + TUDCA, and diabetes + TUDCA + insulin. TUDCA (an inhibitor of ER stress) groups are positive control groups created to compare linagliptin groups in terms of ER stress. Linagliptin and TUDCA were given by oral gavage and 1U insulin was administered subcutaneously for 2 weeks. A significant decrease was observed in the MDA and NOX1 levels and the number of atretic follicles in the ovaries of the diabetes + linagliptin + insulin group compared to the diabetes + insulin group. The use of linagliptin and insulin increased the expression of pro‐survival XBP1s transmembrane protein and decreased the expression of proapoptotic ATF4, pJNK1/2, cleaved caspase 12, and cleaved caspase 3 in mouse ovaries. Our study provides new therapeutic evidence that linagliptin administered in addition to insulin induces ER stress mechanism‐dependent survival in ovaries with type 1 diabetes. Significance Statement: In our study, we aimed to answer the question whether the use of linagliptin, a DPP4 inhibitor with high antioxidant activity, and insulin triggers the survival pathway or the apoptotic pathway of unfolded protein response (UPR) signaling activated by endoplasmic reticulum (ER) stress in type 1 diabetes mellitus (T1DM) mouse ovaries to reach new therapeutic targets. Our results showed that the addition of linagliptin to insulin induced pro‐survival UPR by decreasing ATF4 and increasing XBP1s proteins, while suppressing proapoptotic UPR by decreasing p‐JNK1 + JNK2, cleaved caspase 12, and cleaved caspase 3 proteins. This study will contribute to the literature in terms of the discovery of new methods to be used in the treatment of ovarian pathologies associated with diabetes‐induced ER stress. [ABSTRACT FROM AUTHOR]

Cytoskeletal networks are proteins that effectively maintain cell integrity and provide mechanical support to cells by actively transmitting mechanical signals. Intermediate filaments, which are from the cytoskeleton family and are 10 nanometres in diameter, are unlike actin and microtubules, which are highly dynamic cytoskeletal elements. Intermediate filaments are flexible at low strain, harden at high strain and resist breaking. For this reason, these filaments fulfil structural functions by providing mechanical support to the cells through their different strain‐hardening properties. Intermediate filaments are suitable in that cells both cope with mechanical forces and modulate signal transmission. These filaments are composed of fibrous proteins that exhibit a central α‐helical rod domain with a conserved substructure. Intermediate filament proteins are divided into six groups. Type I and type II include acidic and basic keratins, type III, vimentin, desmin, peripheralin and glial fibrillary acidic protein (GFAP), respectively. Type IV intermediate filament group includes neurofilament proteins and a fourth neurofilament subunit, α‐internexin proteins. Type V consists of lamins located in the nucleus, and the type VI group consists of lens‐specific intermediate filaments, CP49/phakinin and filen. Intermediate filament proteins show specific immunoreactivity in differentiating cells and mature cells of various types. Various carcinomas such as colorectal, urothelial and ovarian, diseases such as chronic pancreatitis, cirrhosis, hepatitis and cataract have been associated with intermediate filaments. Accordingly, this section reviews available immunohistochemical antibodies to intermediate filament proteins. Identification of intermediate filament proteins by methodological methods may contribute to the understanding of complex diseases. [ABSTRACT FROM AUTHOR]

The development and progression of sepsis are multifactorial and influence the immunological, endocrine, and cardiovascular systems of the body. Our knowledge of the key mechanisms involved in the pathogenesis of sepsis has expanded exponentially, yet this still needs to be translated into effective targeted therapeutic regimes. In the present study, we aimed to determine whether resveratrol has positive effects in the experimental sepsis rat model. Twenty‐eight male Spraque–Dawley rats were randomly divided into four groups (n = 7) as follows: control, lipopolysaccharide (LPS) (30 mg/kg dose), resveratrol, and LPS and resveratrol. After the experiment, liver and kidney tissues were collected for histopathological evaluation, blood serums were collected to measure malondialdehyde levels with enyzme‐linked immunosorbent assay, and Toll‐like receptor‐4 (TLR4), tumor necrosis factor‐α (TNF‐α), nuclear factor‐κB (NF‐κB) immunoreactivity density was evaluated immunohistochemically. In addition, messenger RNA expression levels for TLR4, TNF‐α, NF‐κB, interleukin‐1β, and interleukin 6 were measured. In addition, the damage observed in liver and kidney tissue was determined by AgNOR (argyrophilic nucleolar organizer regions) staining. LPS application caused severe tissue damage, oxidative stress, and increased the expressions of proinflammatory proteins and genes we evaluated, while resveratrol application eliminated these negativities. Resveratrol has been proven to suppress the TLR4/NF‐κB/TNF‐α pathway, a possible therapeutic signaling pathway that is important in initiating the inflammatory response in an animal model of sepsis. Significance Statement: Toll‐like receptors (TLRs) are potent activators of the inflammatory response. TLR4 is a potential therapeutic target for sepsis. Resveratrol has a protective role on liver and kidney functions in sepsis via the TLR4/nuclear factor‐κB/tumor necrosis factor‐α signaling pathway. AgNOR (argyrophilic nucleolar organizer regions) staining intensity, which quantifies tissue damage, increased in liver tissues in a lipopolysaccharide‐induced sepsis model. [ABSTRACT FROM AUTHOR]

The aim of this study was to understand the expression of big potassium (BK, KCa1.1) channels in epileptic seizures under magnetic field application. Forty Wistar albino adult male rats were divided into five groups (n = 8). First group rats were control group. Pentylenetetrazole (PTZ) administrated to second group rats to induce the seizures with 35 mg/kg intraperitoneally injection every two days. Levetiracetam (LEV) i.p. at a dose of 108 mg/kg was given to third group rats as positive control group (PC) before 20 minutes PTZ administration. Pulsed magnetic field with 1.5 mT was exposed to the fourth group rats for 3 hours a day for 1 month as magnetic field (MF) group. 1.5 mT pulsed magnetic field was exposed to the fifth group rats for 3 hours a day for 1 month in addition to PTZ administration (PTZ+MF). KCa1.1 not changed in hippocampus of PTZ rats while increased in frontal cortex and pons for PTZ group but not changed with magnetic field exposure. KCa1.1 increased in heart of PTZ animals and turned back to mean control values with magnetic field exposure. Suppressing the expected increase of c-fos protein expression in seizures with magnetic field application but not being able to change the KCa1.1 expression shows that new studies can be done by increasing the frequency of 1.5 mT magnetic field. [ABSTRACT FROM AUTHOR]

Copyright of Turkish Bulletin of Hygiene & Experimental Biology / Türk Hijyen ve Deneysel Biyoloji is the property of Refik Saydam National Public Health Agency and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Tartrazine, an azo dye prevalent in pharmaceuticals and food items, was investigated for its impact on fetal development, specifically examining visceral and skeletal abnormalities in rat offspring exposed to daily oral doses throughout pregnancy. Fourteen pregnant rats were randomly assigned to control and tartrazine groups (seven animals each), with tartrazine administered via oral gavage at 7.5 mg/kg throughout gestation. Offspring were categorized by gender for histopathological and genetic analysis of visceral structures. Bone quality and fracture resistance assessments involved micro‐CT, Raman spectroscopy, and biomechanical testing. Results highlighted distinct internal organ tissue differences in the tartrazine group, notably increased hemorrhagic and inflammatory cell infiltration, degeneration, and vacuolization compared to controls. Gender‐specific alterations in mRNA levels of IL‐6, IL‐1β, TNF‐α, and TRPM2 genes (p < .001) were also noted. Moreover, tartrazine‐exposed groups exhibited reduced trabecular thickness, bone volume, and significant alterations in bone matrix composition and quality alongside significant decreases in fracture resistance (p < 0.05). This study concludes that intrauterine exposure to tartrazine can result in adverse impacts on organ and bone development in rat offspring. [ABSTRACT FROM AUTHOR]

Background Material and methods Results Conclusion Studies for new treatment strategies on cancer continue, and new searches continue in the diagnosis and evaluation of cancer. This study examined the possible anticarcinogenic effect of Rutin on the brain tissues of male mice with Ehrlich ascites carcinoma (EAC).We used micro‐computed tomography (micro‐CT) and histologically Hematoxylin&Eosin (H&E) staining methods for evaluation.In the evaluation results, we saw a significant decrease in the brain volume of the tumor group to the control group. The difference in volume between the Rutin treatment group and the control group was not significant. In the brain tissues of the tumor group, numerous degenerated neurons characterized by pericellular/perivascular space expansion, cell swelling, or expansion were detected in the cortex and hippocampus regions. We showed a reduction in the damage rate in the Rutin treated group.As a result, Rutin was found to have an anticarcinogenic effect. In addition to the classical histological evaluation, we used a newer method, micro‐CT, in our study. We believe that this study has important results both in terms of its originality and adding new information to the literature. [ABSTRACT FROM AUTHOR]

Fetal alcohol syndrome (FAS) can occur because of high amount of alcohol intake during pregnancy and is characterized by both physical and neurological problems. Children diagnosed with FAS have difficulties in learning, memory, and coordination. Hippocampus has a major role in memory and learning. We aimed to determine whether alcohol exposure during pregnancy had any effect on offspring by evaluating learning ability as well as oxidative stress and autophagy in the hippocampus and cortex tissues of litters. Attention was also paid to sex differences. To do so, TRPM2, Beclin1, p62, LC3B, IBA1, parvalbumin, GAD65, and mGluR5 expression levels were evaluated by immunohistochemistry. Lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels, as well as total oxidant (TOS) and total antioxidant (TAS) status were determined by ELISA. Learning experiments were evaluated by the Morris water maze (MWM) test. Our findings demonstrated that IBA1, LC3B, GAD65, and mGluR5 expression levels were higher in female rats of the chronic alcohol exposure (CAE) model. Our IHC results revealed that TRPM2 expression levels were significantly increased in both males and females in the CAE group. Likewise, TAS was lower, and TOS was higher in CAE animals. Moreover, MWM outcomes supported a learning deficiency in CAE litters compared to controls and indicated that female offspring outperformed males in learning experiments. Therefore, our results revealed the detrimental effects of alcohol exposure during pregnancy on autophagy signaling in the hippocampus and cortex tissue of litters, which could affect the learning ability of animals., (© 2024 The Author(s). Environmental Toxicology published by Wiley Periodicals LLC.)

Introduction: Traumatic brain injury (TBI) is one of the major causes of death and disability worldwide, and brings a huge burden on the quality of life of patients with TBI and the country's healthcare system. Peripheral organs, especially the kidney, and liver, may be affected by the onset of molecular responses following brain tissue damage. While secondary injury responses post TBI has been well studied in the brain, the effect/consequences of these responses in the peripheral organs have not yet been fully elucidated. Thus, our study aimed to investigate the immunoreactivity of these responses, particularly via proinflammatory cytokines and autophagy markers in the kidney and liver post-acute and chronic TBI., Material and Methods: Mild TBI (mTBI) and repetitive mTBI (r-mTBI) were induced in male and female 2-month-old Balb/c mice via the Marmarou weight-drop model. Liver and kidney tissues were sampled at 24 hours (acute) and 30 days (chronic) post TBI and subjected to histopathological and immunoreactivity analysis., Results: Interleukin (IL)-6 levels were significantly increased in the male liver and kidney tissues in both TBI groups compared to the control group but were seen to be decreased in the female r-mTBI chronic liver and r-mTBI acute kidney. Tumor necrosis factor a (TNF-a) levels were found to increase only in the female r-mTBI chronic kidney tissue and mTBI chronic liver tissue. IL-1b levels were increased in the male and female r-mTBI liver tissues but decreased in the female mTBI kidney tissue. Inducible nitric oxide synthase (iNOS) levels were found to be significantly increased in the female mTBI acute and r-mTBI chronic kidney tissue and mTBI liver tissue, but decreased in the r-mTBI acute kidney and r-mTBI liver tissues. Beclin-1 levels were increased in male mTBI chronic and r-mTBI acute liver tissue but decreased in the r-mTBI chronic group. LC3A/B and P62/SQSTM1 levels were significantly increased in the female mTBI chronic and male r-mTBI chronic liver tissues but decreased in the male r-mTBI and female r-mTBI acute kidney tissues. Significant histopathological changes were also observed in the liver and kidney tissue which were dependent on the TBI severity, gender, and time post TBI., Conclusions: The results showed that TBI may elicit peripheral molecular responses, particularly in terms of alteration in the levels of inflammatory cytokines and autophagy markers, which were gender- and time-dependent. This suggests that TBI may have a significant role in the cellular damage of the kidney and liver in both the acute and chronic phases post TBI, thus ensuring that the effects of TBI may not be confined to the brain.

The aim of this study was to understand the expression of big potassium (BK, K Ca 1.1) channels in epileptic seizures under magnetic field application. Forty Wistar albino adult male rats were divided into five groups ( n  = 8). First group rats were control group. Pentylenetetrazole (PTZ) administrated to second group rats to induce the seizures with 35 mg/kg intraperitoneally injection every two days. Levetiracetam (LEV) i.p. at a dose of 108 mg/kg was given to third group rats as positive control group (PC) before 20 minutes PTZ administration. Pulsed magnetic field with 1.5 mT was exposed to the fourth group rats for 3 hours a day for 1 month as magnetic field (MF) group. 1.5 mT pulsed magnetic field was exposed to the fifth group rats for 3 hours a day for 1 month in addition to PTZ administration (PTZ+MF). K Ca 1.1 not changed in hippocampus of PTZ rats while increased in frontal cortex and pons for PTZ group but not changed with magnetic field exposure. K Ca 1.1 increased in heart of PTZ animals and turned back to mean control values with magnetic field exposure. Suppressing the expected increase of c-fos protein expression in seizures with magnetic field application but not being able to change the K Ca 1.1 expression shows that new studies can be done by increasing the frequency of 1.5 mT magnetic field.

Purpose: This study was designed to investigate the effect of apilarnil on neuronal damage and related mechanisms in a sepsis model in order to demonstrate whether or not apilarnil has neuroprotective effect., Methods: In this study, 64 adult male Sprague-Dawley species rats were randomly divided into eight groups. The rats were administered apilarnil and/or lipopolysaccharide (LPS). Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), xanthine oxidase (XOD) and testican-1 levels were measured in the brain tissue. Proinflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin 1 beta [IL-1β], interleukin 6 [IL-6]) were measured in brain tissue. Histological examinations were performed on hippocampus and cortex tissues in all groups. Apoptotic cell count was estimated using the Tunel method to observe the apilarnil's effect on apoptosis. Purkinje cells were counted in the hippocampus to measure the protective effect of apilarnil on the hippocampus., Results: Apilarnil reduced the decrease in SOD and CAT levels in the brain developing sepsis. Apilarnil reduced the increase in MDA, XOD, and testican-1 levels in the septic brain. It was observed that the number of degenerated neurons due to sepsis decreased as apilarnil dose increased. Apilarnil reduced the elevated levels of proinflammatory cytokines (IL-6, TNF-α, IL-1β) induced by sepsis. Apilarnil prevented sepsis-related apoptosis in the brain., Conclusion: The neuroprotective potential of apilarnil against brain damage in the sepsis model was demonstrated and suggested that it has the potential to contribute to new therapeutic targets against various neurological disorders.