Abstract

In this study, hepatoprotective activity of CAPE, which has antiinflammatory, anticancer, antiviral, and immunomodulatory effects, was investigated in the CCI4 induced liver injury model in rats. Twenty-one Sprague Dawley rats were divided into the three groups: Control (n=7), CCI4 (n=7), CCI4 + CAPE (n=7). The serum levels of AST, ALT, LDH, and bilirubin were measured on the first and last day (10 th day) in all experimental animals. Histopathological examinations were carried out in the rats sacrificed on the tenth day. For histopathological evaluation, livers of all rats were removed and processed for light microscopy. The levels of unconjugated bilirubin, AST, ALT, ALP in CCI4 group were markedly higher than those in the control group (p<0.01, p<0.01, p<0.001 and p<0.05 respectively). The values of these parameters in CAPE+CCI4 group were lower than those in CCI4 (p<0.01, p<0.05, p<0.05, p<0.001 respectively). Histopathological findings also corfirmed that CCI4 induced hepadic damage and support the wiev that CAPE has a hepatoprotective activity. The results of this study indicate that CAPE has a hepatoprotective action in acute liver injury.

Highlights

  • Numerous substance are known to cause liver damage

  • Sections were stained with hematoxylin and eosin (H&E) and Masson’s trichrome, and examined with a BX50-3 Olympus light microscope (Olympus Optical, Tokyo, Japan)

  • The severe hepatic lesions induced by CCl4 were remarkably ameliorated by Caffeic acid phenethyl ester (CAPE)

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Summary

Introduction

Numerous substance are known to cause liver damage One of these chemicals is carbon tetrachloride (CCl4) which is a xenobiotic that induces hepatotoxicity in humans as well as in animals [1,2]. In vitro studies showed that CAPE is effective against experimentally produced liver toxicity [21] It has antiproliferative and antioxidant properties and has been shown to inhibit lipooxygenase activities as well as suppress lipid peroxidation [23,24,25,26,27]. It was shown in a previous study that CAPE preserved heart tissue from doxorubicin-induced oxidant injury [28]

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