Nitazoxanide mitigates methotrexate hepatotoxicity in rats: role in inhibiting apoptosis and regulating endoplasmic reticulum stress.

Objectives: Hepatotoxicity is a severe outcome of methotrexate (MTX) therapy, limiting its clinical use and contributing to its related morbidity and mortality. This study investigated the hepatoprotective effects of nitazoxanide (NTZ), an antiprotozoal drug, against MTX-induced hepatotoxicity and whether endoplasmic reticulum (ER) stress-modulation underlies the expected beneficial effects of NTZ.

Methods: Thirty-six rats were allocated to six groups, one control group and five MTX groups, where induction of hepatotoxicity was achieved via injecting MTX (20 mg/kg).

Reno- and hepato-protective effect of allopurinol after renal ischemia/reperfusion injury: Crosstalk between xanthine oxidase and peroxisome proliferator-activated receptor gamma signaling.

Renal ischemia/reperfusion (I/R) is a common cause of acute kidney injury and remote liver damage is an ultimate negative outcome. Current treatments for renal I/R typically involve the use of antioxidants and anti-inflammatory to protect against oxidative stress and inflammation. Xanthine oxidase (XO) and PPAR-γ contribute to renal I/R-induced oxidative stress; however, the crosstalk between the two pathways remains unexplored.

Anti-Oxidant and Anti-Inflammatory Effects of Lipopolysaccharide from against Ethanol-Induced Liver and Kidney Toxicity in Experimental Rats.

This study aimed to investigate the protective effects of lipopolysaccharide from (LPS-RS) against ethanol-induced hepatotoxicity and nephrotoxicity in experimental rats. The study involved an intact control group, LPS-RS group, two groups were given ethanol (3 and 5 g/kg/day) for 28 days, and two other groups (LPS-RS + 3 g/kg ethanol) and (LPS-RS + 5 g/kg ethanol) received a daily dose of LPS-RS (800 μg/kg) before ethanol. Ethanol significantly increased the expression of nuclear factor kappa B (NF-κB) and levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the liver tissue and decreased anti-oxidant enzymes.

DNA methylation status of the methylenetetrahydrofolate reductase gene promoter in peripheral blood of end-stage renal disease patients.

End-stage renal disease (ESRD) is one of the main causes of morbidity and mortality worldwide. DNA methylation is a major epigenetic modification of the genome that has the potential to silence gene expression. Methylenetetrahydrofolate reductase (MTHFR) gene inactivation was recognized as a predisposing factor of hyperhomocysteinemia in renal patients.