Abstract

Liver disease is one of the most common causes of death in the world. Nowadays, research studies have been focused on the development of new drugs for treatment of liver damage. Some natural products from medicinal plants have been found as potent agents for protection against liver injury induced by chemicals. Thus, it is interesting to find more effective natural products for protection against liver injury. Accordingly, the present study was designed to assess the hepatoprotective potential of a diterpenoid forskolin, isolated from the Indian plant Coleus forskohlii, at different doses in rat model with acute liver injury induced by carbon tetrachloride (CCl4) at a dose of 1ml/kg intraperitoneally as a mixture with corn oil. Forkolin was administered in doses of 5,10,20,40 mg/kg intraperitoneally for 7 days. Its protective effect was assessed via liver function tests and histopathological liver sections. Significant reduction in the hepatic enzymes levels was found in animals treated with forskolin at a dose of 10mg/kg as well as restoration of hepatocellular architecture. Therefore, treatment with forskolin showed preventive effect against CCl4-induced liver damage.

Highlights

  • Liver disease is a serious health problem throughout the world

  • The 10 mg/kg dose of forskolin showed a significant decrease in ALT and AST reaching 18.6 % and 25.2 % respectively as compared to the CCl4 group (Table 1)

  • Acute and chronic liver diseases constitute a global concern, and it is mostly induced by viral hepatitis, alcoholism, iron overload or drug toxicity

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Summary

Introduction

Liver disease is a serious health problem throughout the world. A special interest in lowering liver damage arises since liver is a vital organ that plays a pivotal role in metabolism and detoxification of various endogenous and exogenous harmful substances (Yang et al, 2010). Despite new advances in hepatology, there is a lack of effective therapeutic strategies or specific medicines for the protection against hepatic disorders (Wu et al, 2007). CCl4 metabolism begins with the highly reactive trichloromethyl free radicals (CCl3·) by the action of the liver reduced nicotinamide adenine dinucleotide phosphate (NADPH) cytochrome P450 enzyme system (McCay et al, 1984). These free radicals are believed to cause lipid peroxidation, and the breakdown of cellular membranes (Manibusan et al, 2007)

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