Study of the Protective Effects of Benfotiamine Against CCl4-Induced Hepatotoxicity in Rats

  • Tavga A. Aziz
  • Zheen A. Ahmed
  • Kasim M. Juma'a
  • Munaf H. Abdulrazzaq
  • Saad A. Hussain
  • Saad A. Hussain

Abstract

Liver is considered as the first target for the toxic effects of toxins and other xenobiotics, and this can be attributed to its role as a site which receive all absorbed xenobiotics from the gastrointestinal tract and its role as a major site for biotransformation of xenobiotics. The present study was designed to evaluate the possible hepatoprotective effect of benfotiamine against CCl4-induced hepatotoxicity in rats. The study was conducted on 48 male albino rats; the animals were allocated into 8 groups (6 rats in each group) and treated as follow: 4 groups treated with oral doses of either normal saline, benfotiamine (100 mg/kg), thiamine (100 mg/kg), N-acetylcystein (400 mg/kg) only without induction of hepatic damage. The other 4 groups were treated as indicated previously with induction of hepatic damage with CCl4; at the end of treatment period, rats were scarified, blood samples obtained and livers excised for the assessment of the oxidative stress parameters (MDA and GSH), cholesterol and triglycerides levels. Additionally, serum levels of total bilirubin, albumin, total protein and the activities of ALT, AST and ALP enzymes were evaluated before and after treatment with benfotiamine. Tissue sections were prepared for evaluation of histopathological changes. The results indicated that benfotiamine has the ability to protect hepatic tissue against the toxicity induced by CCl4, revealed through reduction of serum levels of TSB and liver enzymes, decrease in the hepatic tissue MDA levels and elevation of GSH there. Histological evaluation of tissue sections prepared for this purpose confirmed the previous finding. In conclusion, benfotiamine is capable to protect liver tissue against CCl4-induced toxicity in rats more than thiamine.

Key words: Benfotiamine, CCl4, Hepatotoxicity

Published
2017-03-30

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