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

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 administrati...

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Veröffentlicht in:Processes 2022-01, Vol.10 (1), p.31
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description 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.
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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 &lt; 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 &lt; 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.</description><identifier>ISSN: 2227-9717</identifier><identifier>EISSN: 2227-9717</identifier><identifier>DOI: 10.3390/pr10010031</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Acids ; Alanine ; Alanine transaminase ; Albumin ; Albumins ; Alzheimer's disease ; Animals ; Antioxidants ; Aspartate aminotransferase ; Carbon ; Carbon tetrachloride ; Catalase ; Chemicals ; Chlorogenic acid ; Cholesterol ; Enzymes ; Experiments ; Glutathione ; Glutathione peroxidase ; Glutathione reductase ; Hepatotoxicity ; Histopathology ; Injury prevention ; Laboratories ; Lipid peroxidation ; Lipids ; Liver ; Olive oil ; Oral administration ; Oxidative stress ; Pathogenesis ; Peroxidase ; Reductases ; Serum levels ; Signal transduction ; Silymarin ; Superoxide dismutase ; Thiobarbituric acid ; Transaminases ; Triglycerides ; Variance analysis</subject><ispartof>Processes, 2022-01, Vol.10 (1), p.31</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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subjects Acids
Alanine
Alanine transaminase
Albumin
Albumins
Alzheimer's disease
Animals
Antioxidants
Aspartate aminotransferase
Carbon
Carbon tetrachloride
Catalase
Chemicals
Chlorogenic acid
Cholesterol
Enzymes
Experiments
Glutathione
Glutathione peroxidase
Glutathione reductase
Hepatotoxicity
Histopathology
Injury prevention
Laboratories
Lipid peroxidation
Lipids
Liver
Olive oil
Oral administration
Oxidative stress
Pathogenesis
Peroxidase
Reductases
Serum levels
Signal transduction
Silymarin
Superoxide dismutase
Thiobarbituric acid
Transaminases
Triglycerides
Variance analysis
title Protective Effects of Chlorogenic Acid against Carbon Tetrachloride-Induced Hepatotoxicity in Mice
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