Protective Effects of Chlorogenic Acid against Carbon Tetrachloride-Induced Hepatotoxicity in Mice

Yu-Wen Hsu,Ya-Yu Chen,Chia-Fang Tsai

doi:10.3390/pr10010031

Abstract

The protective effects of chlorogenic acid (CGA) against liver injury were evaluated by its reduction in carbon tetrachloride (CCl4)-induced hepatic damage in ICR mice. The animals were orally given CGA (60, 100, and 200 mg/kg, respectively) or silymairn (200 mg/kg) daily with 0.3% CCl4 administration (3 mL/kg, dissolved in olive oil) after medicament treatment on the 7th day. Compared with the normal group, CCl4 caused severe impairment in liver according to the evidence of significant reduction in the level of total albumin and expansion (p < 0.05) of the activities in aspartate aminotransferase (AST) and alanine aminotransferase (ALT), cholesterol, triglyceride (TG), and total albumin in serum, decreased the level of glutathione (GSH), and diminished the activities of catalase, superoxide dismutase (SOD), glutathione reductase (GSH-Rd), and glutathione peroxidase (GSH-Px) in liver while increasing the level of hepatic thiobarbituric acid-reactive substances (TBARS). However, oral administration of CGA or silymarin could significantly (p < 0.05) decrease the serum levels of AST, ALT, cholesterol, TG, and total albumin and elevated the serum total albumin and the activities of GSH, catalase, SOD, GSH-Rd, and GSH-Px while leading to decline the TBARS in liver compared with CCl4-intoxicated group. Moreover, histopathology displayed that CGA decreased the formation of lesions in liver resulted from CCl4. The outcomes indicate that CGA shows the efficiency hepatoprotective consequences for CCl4-incited liver injuries in mice by the elevation of the activities of antioxidant enzymes and hindrance of lipid peroxidation.

Highlights

There are many hepatotoxins in life, such as ethanol in alcoholic beverages, acetaminophen in antipyretic and analgesic drugs, and carbon tetrachloride (CCl4 ) in chemicals, which could cause liver damage and are characterized by causing various degrees of degeneration and death of hepatocytes [1]
The conjugated combination of trichloromethyl radicals, a metabolite of CCl4 in the liver, with hepatocyte proteins is the initial step of the liver injury process, which subsequently results in lipid peroxidation of membrane, and to hepatocyte necrosis [6]
There was a remarkable increase (p < 0.05) of serum activity of AST, ALT, and total albumin in CCl4 treated group when contrasted with normal controls (Table 1), demonstrating that CCl4 induced hepatotoxicity

Summary

Introduction

There are many hepatotoxins in life, such as ethanol in alcoholic beverages, acetaminophen in antipyretic and analgesic drugs, and carbon tetrachloride (CCl4 ) in chemicals, which could cause liver damage and are characterized by causing various degrees of degeneration and death of hepatocytes [1]. Many studies suggested that CCl4 has been proven to be a hepatoxin that effectively induces liver damage in hepatopathy animal models, and has been widely used in experiments [4,5]. It is known that natural antioxidants have specific functions to scavenge ROS and diminish lipid peroxidation, so they can effectively prevent liver pathologies related to oxidative stress [2,7]. A main defense strategy of effective prevention and treatment liver pathologies include diminishing the manufacture of reactive metabolites and inhibiting lipid peroxidation by promoting the levels of effective member of the antioxidant defense system, e.g., catalase, glutathione (GSH), and superoxide dismutase (SOD) [8,9,10]

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