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We aimed to analyze the effects of diacerein in a rat model of partial unilateral ureteral obstruction (PUUO).

Copyright of Turkish Journal of Trauma & Emergency Surgery / Ulusal Travma ve Acil Cerrahi Dergisi is the property of KARE Publishing 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.)

This study aims to evaluate the protective efficacy of remifentanil against testicular ischemia-reperfusion injury.The study included 24 male rats. The rats were randomized into three groups: Group 1 was the control group. Group 2 was subjected to a testicular torsion/detorsion model. Group 3 underwent similar procedures and additionally received remifentanil (0.6 μg/kg/min) intravenously for the first 20 min of reperfusion. Blood samples were taken for biochemical analyses, and orchiectomy was performed for histopathologic examination.Biochemical analysis of blood samples showed a significant increase in antioxidant enzyme activity, including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in Group 3 compared to Group 2 (p:0.004 and p:0.002, respectively). There was a dramatic decrease in the levels of proinflammatory cytokines, including interleukin-1 beta (IL-1 Beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in Group 3 compared to Group 2 (p:0.001, p:0.046, and p:0.004, respectively). Similarly, malondialdehyde (MDA) levels decreased in Group 3 compared to Group 2 (p:0.004). Histopathologic examination of Group 3 rats showed positive changes in inflammation, hemorrhage, edema, and congestion levels compared to Group 2 (p<0.001). Similarly, there was a positive effect on the Johnsen and Cosentino score in Group 3 compared to Group 2 (p:0.001 and p<0.001, respectively).In our study, it has been documented that remifentanil protects against testicular ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

This study aims to investigate the curative effects of Morin, a flavonoid, against arsenic toxicity in 3T3 embryonic fibroblast cells and its effect on the molecular mechanisms of cells. The cytotoxicity and viability of the cells were measured by MTT and LDH tests. Arsenic (0.74 μM) was used to trigger toxicity and Morin (50 μM) was used for treatment. The levels of oxidative stress biomarkers and the activities of antioxidant enzymes were measured by spectrophotometric method, and inflammatory markers were measured by ELISA method. While mRNA expression levels of Bax, Bcl-2 levels, and Caspase-3 activity were measured by qRT-PCR technique, TUNEL staining was performed to detect DNA breaks and DAPI staining to visualize nuclear changes. Protein structures were retrieved from the protein data bank. OpenBabel and Autodock programs were used for the molecular docking study. Morin rescued the 3T3 embryonic fibroblast cells exposed to arsenic. However, Arsenic decreased the activities of antioxidant enzymes in cells and significantly increased oxidative stress, inflammation, and apoptosis. Morin treatment reduced oxidative damage and TNF-α and IL-1β levels. Arsenic-induced Caspase-3 mRNA expression level and Bax protein mRNA expression level were significantly increased, while Bcl-2 mRNA expression level was significantly decreased. While Caspase-3 mRNA expression level and Bax protein mRNA expression level decreased with morin treatment, Bcl-2 mRNA expression level increased significantly. Molecular docking study results showed good binding affinity of morin in SOD, GSH-Px, Bax, Bcl-2, Caspase-3, TNF-α, and IL-1β structures. Morin showed antioxidant, anti-inflammatory, and anti-apoptotic effects against Arsenic-induced cellular toxicity. [ABSTRACT FROM AUTHOR]

BACKGROUND: This study investigates the protective effects of etomidate against oxidative damage in an experimental model of ovarian ischemia-reperfusion injury. METHODS: A total of 24 female rats were randomized into three groups. Group 1 served as the control. Group 2 underwent an ovarian torsion/detorsion procedure. Group 3 underwent similar procedures as Group 2; additionally, 4 mg/kg of etomidate was administered intraperitoneally 30 minutes before ovarian detorsion. Blood samples were analyzed for lipid peroxidation, pro-inflammatory cytokine levels, and antioxidant enzyme activity.Furthermore, histopathological scoring was performed to evaluate tissue damage in the ovaries. RESULTS: Biochemical analysis of blood samples revealed reductions in pro-inflammatory cytokines, including interleukin-1 Beta (IL1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), in Group 3 compared to Group 2 (p=0.005, p=0.016, and p<0.001, respectively). Additionally, a decrease in malondialdehyde (MDA) levels was observed in Group 3 compared to Group 2 (p<0.001). In contrast, activities of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), were significantly increased in Group 3 compared to Group 2 (p=0.031 and p=0.001, respectively). Furthermore, Group 3 demonstrated notable reductions in histopathological scores for follicular degeneration, vascular occlusion, bleeding, and inflammation compared to Group 2 (p<0.001, p<0.001, p<0.001, and p=0.001, respectively). CONCLUSION: Etomidate alleviates ischemia-reperfusion injury in a rat ovarian torsion-detorsion model by improving both histopathological and biochemical outcomes. [ABSTRACT FROM AUTHOR]

Copyright of Turkish Journal of Trauma & Emergency Surgery / Ulusal Travma ve Acil Cerrahi Dergisi is the property of KARE Publishing 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.)

Purpose: Colorectal cancer (CRC) is one of the most common and fatal malignancies in humans, still leading to serious morbidity and mortality. We here aimed to investigate the effects of flavonoid apigenin, which is considered to have anti-tumoral activity on CRC with high epidemiological prevalence, on cell proliferation and cell survivals, and the positive and negative dose-dependent effects of genetic or mutational alterations in SWH pathway components on HT29 CRC cell lines. Methods: Human colon cancer cell lines HT-29 were commercially available. In each flask, 5 groups were formed, each of which consists of 5,000 cells for different dose groups and the cells were plated. After a 24 and 48 h incubation period, cytotoxicity values were measured by MTT assay and gene expression was assessed by real-time polymerase chain reaction (PCR) analysis method. Results: Application of 12.5 and 25 nM of apigenin significantly increased cell death in HT29 cell lines. LATS1, STK3 and TP53 gene expression decreased in the same dose groups compared to control and other groups. Conclusion: It has been concluded that TP53 gene is strongly correlated with LATS1 and STK3 genes among the SWH pathway factors in the progression of CRC and could be used as an important marker for early detection of malignant transmission. In addition, it may be effective in CRC cases especially when 25 nM of apigenin applies for therapeutic purpose. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to evaluate the relationship between the preoperative neutrophil-lymphocyte ratio (NLR) and lymph node metastasis and lymph node density after radical cystectomy in patients with invasive urinary bladder cancer. Materials and Methods: Data of 89 patients who underwent radical cystectomy were examined. Our study included only cases with stage 2 urothelial bladder cancer. They were classified according to the lymph node status based on the surgical specimen. Patients with negative results were classified as group 1 and those with positive results as group 2. Patients in group 2 were further evaluated in two subgroups according to their lymph node density. Accordingly, group 2A consisted of patients with lymph node density of <20%, and group 2B involved those with lymph node density of =20%. Groups were compared statistically according to NLR. Results: Of the patients, 71 (79.8%) were male. The patients' mean ages and neutrophil and lymphocyte counts were 67.36±8.64 years, 6.89±3.02 K/µL, and 3.08±2.18 K/µL, respectively. NLRs of groups 1 and 2 were 2.80±2.25 and 4.59±2.97, respectively. The relationship between group 1 and 2 tumors was significant (p=0.008). NLR values were 3.82±2.49 and 5.20±3.25 in groups 2A and 2B, respectively. However, no significant relationship was found between these values (p=0.235). Conclusion: Although no positive correlation was found between NLR and lymph node density, we think that this inflammation marker is an invaluable parameter to predict lymph node metastasis. [ABSTRACT FROM AUTHOR]

Several chemicals, including environmental toxicants and clinically useful drugs, cause severe cellular damage to different organs of our body through metabolic activation to highly reactive substances such as free radicals. Carbon tetrachloride is an organic compound of which chemical formula is CCl₄. CCl4 is strong toxic in the kidney, testicle, brain, heart, lung, other tissues, and particularly in the liver. CCl4 is a powerful hepatoxic, nephrotoxic and prooxidant agent which is widely used to induce hepatotoxicity in experimental animals and to create hepatocellular carcinoma, hepatic fibrosis/cirrhosis and liver injury, chemical hepatitis model, renal failure model, and nephrotoxicity model in recent years. The damage-causing mechanism of CCl4 in tissues can be explained as oxidative damage caused by lipid peroxidation which starts after the conversion of CCl4 to free radicals of highly toxic trichloromethyl radicals (•CCl₃) and trichloromethyl peroxyl radical (•CCl₃O2) via cytochrome P450 enzyme. Complete disruption of lipids (i.e., peroxidation) is the hallmark of oxidative damage. Free radicals are structures that contain one or more unpaired electrons in atomic or molecular orbitals. These toxic free radicals induce a chain reaction and lipid peroxidation in membrane-like structures rich in phospholipids, such as mitochondria and endoplasmic reticulum. CCl4-induced lipid peroxidation is the cause of oxidative stress, mitochondrial stress, endoplasmic reticulum stress. Free radicals trigger many biological processes, such as apoptosis, necrosis, ferroptosis and autophagy. Recent researches state that the way to reduce or eliminate these CCl4-induced negative effects is the antioxidants originated from natural sources. For normal physiological function, there must be a balance between free radicals and antioxidants. If this balance is in favor of free radicals, various pathological conditions occur. Free radicals play a role in various pathological conditions including Pulmonary disease, ischemia / reperfusion rheumatological diseases, autoimmune disorders, cardiovascular diseases, cancer, kidney diseases, hypertension, eye diseases, neurological disorders, diabetes and aging. Free radicals are antagonized by antioxidants and quenched. Antioxidants do not only remove free radicals, but they also have anti-inflammatory, anti-allergic, antithrombotic, antiviral, and anti-carcinogenic activities. Antioxidants contain high phenol compounds and antioxidants have relatively low side effects compared to synthetic drugs. The antioxidants investigated in CCI4 toxicity are usually antioxidants from plants and are promising because of their rich resources and low side effects. Data were investigated using PubMed, EBSCO, Embase, Web of Science, DOAJ, Scopus and Google Scholar, Carbon tetrachloride, carbon tetrachloride-induced toxicity, oxidative stress, and free radical keywords. This study aims to enlighten the damage-causing mechanism created by free radicals which are produced by CCl4 on tissues/cells and to discuss the role of antioxidants in the prevention of tissue/cell damage. In the future, Antioxidants can be used as a therapeutic strategy to strengthen effective treatment against substances with high toxicity such as CCl4 and increase the antioxidant capacity of cells. – CCl4 is free radical source and a strong toxic substance. – CCl4 is the cause of oxidative stress, mitochondrial stress, endoplasmic reticulum stress. – Promising targets have been reviewed in reducing and treating the toxicity of CCl4. – Antioxidant compounds react with free radicals from CCl4 and are involved in reducing cell damage. Thus, antioxidant intake can help maintain normal physiological function. [ABSTRACT FROM AUTHOR]