Aflatoxins are common food contaminants threating human and animal health. Aflatoxin B1 (AFB1) toxication can lead to important health issues. Recent studies have revealed the therapeutic effect of curcumin (Cur) and have drawn attention in the pharmaceutical industry. The therapeutic efficacy of Cur on AFB1-induced oxidative stress, pro-inflammatory response, and hepatorenal damage has not been adequately studied. This study was conducted to evaluate the protective efficacy of Cur on several lipid peroxidation and antioxidant defense system enzymes, some pro-inflammatory cytokines, and liver function tests in rats suffering from chronic aflatoxicosis induced by AFB1 administered for sixty days. Rats were divided into five groups; Control (K), Dimethyl sulfoxide (D), Curcumin (Cur; 300 mg/kg/day, orally), AFB1 (AF; 250 μg/kg/day, oral) and AFB1+ Curcumin (AF + Cur). Oxidative stress caused by AFB1 caused an increase in Malondialdehyde (MDA), a lipid peroxidation product, and a decrease in glutathione (GSH) and superoxide dismutase (SOD) activities. In addition, AFB1 led to increased levels of pro-inflammatory cytokines such as tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), and interleukin-6 (IL-6). Liver function tests after chronic exposure to AFB1 showed that this toxic substance causes liver damage. Concomitant Cur administration normalized AFB1-induced oxidative damage, inflammatory response, and liver functions. This therapeutic effect of Cur on AFB1 was thought to be related to its antioxidant and anti-inflammatory activities. Our results suggest that CUR supplementation in food as it shows beneficial effects particularly on liver impairment exerted by AFB1.

Gentamicin is an aminoglycoside antibiotic with a rapid bactericidal effect on the treatment of many infections. However, its use at high concentrations for more than 7 days causes nephrotoxic side effects. This study investigated the potential of Resatorvid and alpha lipoic acid (ALA) in mitigating gentamicin‐induced nephrotoxicity in rats, considering biochemical, histopathological, and molecular parameters. This study randomly distributed 34 Wistar albino rats into four groups: healthy control (n = 6), Gentamicin (80 mg/kg, n = 7), Gentamicin + Sham (%10 hydroalcoholic solution, n = 7), Gentamicin + Resatorvid (5 mg/kg, n = 7), and Gentamicin + ALA (100 mg/kg, n = 7). Resatorvid treatment led to a statistically significant decrease in urinary IL‐18, KIM‐1, and NGAL levels, whereas ALA treatment significantly reduced KIM‐1 levels compared to the gentamicin‐only group. Both Resatorvid and ALA showed partial reductions in urine creatinine levels. Moreover, treatments with Resatorvid and ALA resulted in statistically significant decreases in NRF‐2, CAS‐3, and NR4A2 expressions. However, only Resatorvid demonstrated a statistically significant decrease in NF‐B expression. These findings highlight the potential of Resatorvid in ameliorating gentamicin‐induced nephrotoxicity, thereby expanding the therapeutic utility of gentamicin and enhancing its efficacy against infections.

This study was designed to investigate the possible protective efficacy of Nigella sativa essential oil against acrylamide induced liver toxicity. Four groups of 32 male Wistar albino rats were formed. Control group was used as a control. acrylamide was administered to the rats in Group AA by gavage at a daily dose of 40 mg/kg. 10mg/kg dose of Nigella sativa essential oil was administered intraperitoneally to the rats in Group NS. In Group AA+NS, daily acrylamide and Nigella sativa essential oil applications were carried out simultaneously as mentioned above. The trial period lasted 15 days. While acrylamide increased malondialdehyde levels in liver tissue, it decreased glutathione and superoxide dismutase levels. In addition, liver pro-inflammatory cytokine levels increased due to acrylamide administration, while anti-inflammatory cytokine levels decreased due to acrylamide administration.: Concomitant administration of Nigella sativa essential oil with acrylamide significantly reduced oxidative stress and inflammation in liver tissues. In conclusion, our findings emphasized that Nigella sativa essential oil has a potential therapeutic role to prevent acrylamide-induced hepatotoxicity.

The primary objective of this study was to investigate the adverse effects of Bisphenol-A (BPA) on the central and peripheral nervous systems at molecular, histopathological, and immunohistochemical levels, as well as to evaluate the potential neuroprotective effects of Nigella Sativa seed oil (NSO). Rats were administered BPA at a dosage of 100 mg/kg body weight per day via gavage for 30 days, alongside NSO at a dosage of 5 ml/kg body weight per day for the same duration. Rats were sacrificed 24 h after the final administration, and molecular, histopathological, and immunohistochemical examinations were conducted on brain and sciatic nerve tissues. BPA exposure resulted in neurotoxic effects in both the central nervous system (brain) and peripheral nervous system (sciatic nerve), leading to oxidative stress, apoptosis, and neurodegeneration. Specifically, glutathione (GSH) levels decreased, while malondialdehyde (MDA) levels increased in both tissues due to BPA administration. Additionally, BPA elevated the gene expression levels of nuclear factor erythroid 2–related factor 2 (Nrf2), Caspase-3, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) mRNA transcripts, while decreasing the expression of nuclear receptor subfamily 4 group A member 2 (NR4A2). In contrast, NSO administration alongside BPA increased GSH content in both tissues and significantly reduced MDA levels. Moreover, NSO decreased the gene expression levels of Nrf2, NF-κB, and Caspase-3 mRNA transcripts, while increasing NR4A2 expression. Furthermore, the neurodegenerative manifestations induced by BPA—such as neuronal degeneration, necrosis, neuronophagy, hemorrhage, gliosis, and elevated glial fibrillary acidic protein (GFAP) levels in the brain—were mitigated by the concurrent administration of NSO, indicating its neuroprotective efficacy. In conclusion, this study provides promising evidence that NSO may therapeutically alleviate BPA-induced neurodegeneration.