Crocin mitigates carbon tetrachloride-induced liver toxicity in rats

Carbon tetrachloride [CCl4] is one of the most dangerous hepatotoxic environmental pollutants thus this study aimed at investigating the potential preventive effect and mechanism of crocin against CCl4- induced hepatotoxicity. Forty Male rats were allocated for two weeks treatment with; corn oil, CCl4 in corn oil, crocin [100 mg/kg], or crocin plus CCl4. At time of euthanasia liver was removed, weighted and processed for histopathological evaluation and estimation of liver contents of active caspase3, lipid peroxidation [MDA] and reduced glutathione [GSH]. We also evaluated antioxidant enzymes activities [superoxide dismutase [SOD], glutathione peroxidase [GSH-Px] and catalase [CAT]], phase I metabolizing enzyme [cytochrome P450 sub family 2E1 [CYP2E1]] an Phase II metabolizing enzyme, [glutathione-S-transferase [GST]] in liver tissue. Blood samples were used for evaluation of liver function tests and inflammatory cytokines [interleukin 6 [IL-6] and tumor necrosis factor alpha [TNF-alpha]]. CCl4 induced significant [p < 0.001], increase in: relative liver weight to body weight, liver MDA content, liver active caspase-3 and plasma levels of IL-6 and TNF alpha. In addition, CCl4 disturbed liver histology, liver metabolizing enzymes [CYP2E1 and GST], and liver function tests [aspartate aminotransferase, alanine aminotransferase, total bilirubin and alkaline phosphatase]. CCl4 induced significant decrease in activities of SOD, CAT, GSH-Px and GSH content. Administration of crocin with CCl4 mitigated all CCl4-disturbed parameters and preserved liver histology close to normal. Crocin ameliorated CCl4-induced liver injury via inhibition of inflammatory cytokines, caspase3 and oxidative stress along with modulation of liver metabolizing enzymes favoring elimination of CCl4 toxic metabolite

Histological study of the effect of simvastatin on the skeletal muscle fibers in albino rat and the possible protective effect of coenzyme Q 10

Simvastatin is a lipid lowering agent. It reduces risk of mortality in persons with coronary heart disease. Some patients treated with simvastatin, have developed liver, kidney and skeletal muscle symptoms. Coenzyme Ql0 has a significant antioxidant activity acting as a primary scavenger of free radicals and influences membrane stability in many tissues including skeletal muscle. Was to evaluate the effect of simvastatin drug on the histological structure of skeletal muscle fibers of adult male albino rats and the possible role of coenzyme Q10 [C0Q 10] as a protective agent. 38 adult male albino rats were used and divided into three groups. Group I [control], group II included 10 rats treated with simvastatin for 4 and 12 weeks and group III included 10 rats treated with simvastatin and CoQ 10 orally for 4 and 12 weeks. The gastrocnemius muscle was dissected and prepared for light and electron microscopic study. In rats subjected to high therapeutic dose of simvastatin for 4 and 12 weeks, the gastrocnemius muscle showed variation in size, splitting and focal degeneration of myofibers as well as mononuclear cellular infiltration and increased deposition of collagen fibers in-between muscle fibers. EM revealed mitochondrial degeneration and dilatation of sarcoplasmic reticulum. Mitochondria were markedly accumulated between myofibrils and in subsarcolemmal space. Coadministration of coenzyme Q 10 with simvastatin for 4 and 12 weeks ameliorated most of the above mentioned histological changes in the animals used. Simvastatin drug caused skeletal muscle damage. Coenzyme Q 10 resulted in protection of the skeletal muscle fibers when given concomitantly with simvastatin