Vitamin E is a potent regulator of inflammatory cytokines released during hepatic toxicity in rats

Document Type : Original Article


Department of Clinical Pathology, Faculty of Veterinary Medicine, Benha University, Moshtohor, Toukh


Paracetamol is a the most utilized analgesic and antipyretic drug, but it may induce hepatotoxicity at increased doses. So, we design this experiment to study the hepatotoxic effect of paracetamol and to detect the role of vitamin E in the alleviation of this toxic effect.
Forty Wistar male rats were classified into 4 groups (10 rats per group); Control (distilled water), Vitamin E (100 mg/kg b. wt. orally for four weeks), Paracetamol (1000 mg/kg b. wt. orally for 3 consecutive days), Vitamin E plus Paracetamol (100 mg vitamin E/kg b. wt. orally for four weeks followed by a dose of paracetamol 1000 mg/kg b. wt. orally daily for 3 consecutive days). Blood and hepatic specimens were collected at the end of treatment. Erythrogram, leukogram, liver enzymes, MDA and expressions of IL-1β, IL4, MCP-1 and TGF mRNA were determined. Also, tissue sections from liver was examined histopathologically.
Paracetamol caused damage of liver tissue indicated by significant increase in the serum ALT and AST activities with a significant decrease in the levels of serum total protein and albumin. Moreover, paracetamol produced a significant elevation in the level of liver malondialdehyde and significant upregulations in the pro-inflammatory biomarkers expression in the hepatic homogenate. The hepatic tissue revealed severe inflammation and hepatic damage. However, vitamin E alleviated the oxidative stress and the hepatotoxicity induced by paracetamol.            
Our experiment revealed that Paracetamol is a hepatotoxic drug in rats. Meanwhile, vitamin E reverses that harmful hepatotoxic effects produced by Paracetamol.


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