Rutin Protects Against Nonylphenol-Induced Reproductive Injury in Rats Via Modulation of Steriogenic, Inflammatory and Apoptotic Pathways

Therapeutic potential of flavonoids and rutin against inflammation-induced on a huntington animal model

This study tested the hypothesis that flavonoids (diosmine, hesperidin and rutin®) play a protective role in the brain and duodenum against 3-Nitropropionic acid (3-NPA) free radical induced inflammation. This was achieved by measuring the levels of GABA, 5-HIAA, dopamine and some inflammation and oxidative stress markers. Male young Wistar rats (weight 60g) received Salmonella thyphimurium ATCC14028 1x106 CFU/g every week, for two consecutive weeks, plus the following treatments: group A, 0.9% NaCl (Control); group B, diosmine (300 mg) + hesperidin (33.3g) + rutin (150 mg/kg); group C, 3-NPA; group D, 3-NPA + mix of flavonoids with 1 ml of rutin® per rat. 3-NPA administration was at 24 mg/kgW by intraperitoneal route and the flavonoids were orally administered at every 48 hours for 15 days. At the moment of euthanasia, the blood was obtained to assess Interleukine-6, glucose, triglycerides and hemoglobin levels. Brain and duodenum were obtained to measure GABA, dopamine, 5-HIAA, lipoperoxidation, reduced glutathione (GSH), total ATPase concentrations and catalase activity using validated methods. The brains, stomach and duodenum were dissected for histological analysis. In group A, there is a decrease in interleukine-6 levels (p = 0.009). In the cortex region of animals in group C, dopamine experienced a significant decrease (p = 0.012). GABA increased (p = 0.001) in cerebellum regions of animals in the groups A, B and C. ATPase activity increased (p = 0.013) in cerebellum regions in animals of groups C and D. Lipoperoxidation diminished (p = 0.043) in cerebellum region of group D. Catalase activity diminished (p = 0.043) in Cortex region of animals in groups B and D, and (p = 0.002) in cerebellum region of animals in groups A and B. Besides, histological changes revealed marked lesions of neuronal cells in experimental animals treated with nitro propionic acid. The protective role of flavonoids and rutin compounds on inhibition of the inflammatory response and correction of the fundamental oxidant/antioxidant imbalance in animals suffering from Huntington diseases are important vistas for further research.

Asiatic Acid Ameliorates Chlorpyrifos-Induced Toxicity in Rats: Biochemical and Histopathological Insights

ABSTRACT Introduction: Chlorpyrifos (CPF), one of the most widely used organophosphorus (OP) insecticides, exerts its toxic effects in part by inducing oxidative stress. Despite increasing recognition of natural antioxidants as potential countermeasures, the efficacy of asiatic acid (AA), a bioactive triterpenoid from Centella asiatica, against CPF-induced toxicity remains unexplored. This study aimed to investigate the protective effects of AA against CPF-incuded toxicity model in rats by analyzing biochemical and histological parameters in serum, liver, and brain tissues. Material and Methods: Adult male Sprague Dawley rats (n=30) were randomly divided into five groups: control, CPF (279 mg/kg, subcutaneously), and three AA-pretreated groups (35, 70, and 140 mg/kg, per os) for 14 days prior to CPF exposure. Oxidative stress markers [malondialdehyde (MDA), advanced oxidation protein products (AOPP)] and antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx)] were measured in serum, liver, and brain. Histopathological and immunohistochemical analyses assessed tissue injury and apoptotic responses. Results: AA administration significantly attenuated CPF-induced oxidative damage and restored antioxidant defenses in a dose-dependent manner. Histopathological analyses confirmed that AA mitigated hepatic and neuronal damage and preserved tissue architecture. Immunohistochemistry revealed that AA suppressed CPF-induced upregulation of the pro-apoptotic protein Bcl-2-associated X protein (Bax), indicating reduced apoptosis. Conclusion: This study provides the first demonstration that AA exerts robust systemic antioxidative, hepatoprotective, and neuroprotective effects against CPF-induced toxicity. These findings highlight AA’s therapeutic potential for mitigating organophosphate pesticide poisoning, warranting further translational research. Keywords: Asiatic acid, chlorpyrifos, hepatoprotection, neuroprotection, organophosphate toxicity, oxidative stress

Urtica dioica L. Alleviates Bisphenol A-Induced Testicular Toxicity in Rats via Modulation of Oxidative Stress, Inflammation, and Apoptosis

Simple Summary Exposure to food contaminants is considered one of the significant environmental risk factors that play a role in the etiology of male infertility. Bisphenol A (BPA), which is widely found in the composition of plastic products, holds a significant place among foodborne contaminants. Plants with high antioxidant capacity are frequently used for their protective effects against the toxic effects caused by BPA, which can act as an endocrine-disrupting chemical. The aim of this study was to evaluate the protective and ameliorative effects of Urtica dioica L. (UD) against BPA-induced testicular dysfunction. The findings indicate that UD treatment significantly reduced the adverse effects of BPA on the male reproductive system through antioxidant, anti-inflammatory, and antiapoptotic mechanisms. These findings suggest that UD could be considered a potential pharmacological agent in the treatment of infertility caused by BPA exposure.

Molecular insights into the protective role of nano-naringin in mancozeb-induced testicular damage and infertility

Mancozeb (MZ) is an extensively used fungicide with well-documented reproductive toxicity induced by oxidative stress and hormonal disruption. Antioxidants such as naringin (NAR) have been studied as protective agents, but their therapeutic application is limited by poor bioavailability. Nano-formulated approaches, including chitosan-coated nanoparticles (NARNPs), offer a promising strategy to enhance delivery and efficacy. The present study explores this concept by evaluating the protective effects of NAR and NARNPs against MZ-induced testicular damage and infertility in rats. 42 adult male albino Wistar rats were divided into six groups (n = 7) as follows: (1) control, (2) NAR (20 mg/kg bwt), (3) NARNPs (20 mg/kg bwt), (4) MZ (250 mg/kg bwt), (5) NAR + MZ, and (6) NARNPs + MZ. Data revealed that the exposure of rats to MZ caused a significant decrease in the body weight gain, sperm viability and motility, serum testosterone level, and testicular antioxidant enzyme activities, along with an increase in the lipid peroxidation. MZ also inhibited the expression of steroidogenic genes and proliferating markers in testes. The administration of NAR with MZ partially restored oxidative homeostasis and the reproductive biomarkers. Otherwise, NARNPs were more effective than NAR, which substantially improved the testicular morphology and function, as well as partially returned the gene expression back to normal with higher immunoexpression of proliferating markers in testicular tissues. The study highlights the potential of nano-formulated NAR as a promising strategy to counteract MZ-induced reproductive damage and improve testicular health via enhancing steroidogenic gene expression.

Ameliorative effect of vinpocetine on brain toxicity in rats treated with acrylamide

Background: Acrylamide (AC) is a highly reactive carbonyl compound widely used in industrial processes, having oxidative stress, neurotoxicity, and genotoxicity properties. Vinpocetine has been reported to exhibit neuroprotective, antioxidant, and anti-inflammatory properties. Aim: The study aims to evaluate vinpocetine’s protective effects in mitigating AC-induced toxicity in male albino rats. Methods: In the current research, 24 rats were used, arranged into 4 groups as follows: normal untreated group, Vinpo. group (5 mg/kg b.wt), AC group (38.27 mg/kg b.wt), Vinpo. + AC group (received Vinpo. and after one hour received a dose of AC). At the end of the experimental period, blood samples and brain specimens were collected from each rat to assess hematological and biochemical parameters and to conduct histopathological and immunohistochemical analyses. Results: AC administration caused a marked reduction in hematological parameters, reduced glutathione (GSH), superoxide dismutase (SOD), and brain-derived neurotrophic factor (BDNF). Also resulted in a marked reduction in key neurotransmitters (serotonin, dopamine, and acetylcholine (ACH)) as an indicator for oxidative stress and toxicity. Lipid peroxidation markers, like malondialdehyde (MDA), increase as an indicator of oxidative injury. The histological structural abnormalities and enhancement in the level of cleaved caspase-3 indicated the damage in brain tissues. Conclusion: Vinpocetine administration ameliorated hematological disturbances, oxidative damage, and histological alterations resulting from AC administration. These findings suggest that vinpocetine has a protective action against AC-induced neural damage.

Protective effect of resveratrol against sub-acute diazinon-induced oxidative stress in rat kidney