Effect of autophagy inhibitor chloroquine on acute alcoholinduced liver disease.
10.12047.j.cjap.5551.2018.025
- Author:
Wen-Hua SANG
1
;
Mei-Chun ZENG
1
;
Sha CHEN
1
;
Ran CHEN
1
;
Xiao-Fang FAN
1
;
Yong-Sheng GONG
1
;
Hai-Lin ZHANG
2
;
Hong-Yu ZHANG
3
;
Xiao-Xia KONG
1
Author Information
1. School of Basic Medicine, Institute of Hypoxia Research, Wenzhou 325035, China.
2. The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou 325035, China.
3. School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
- Publication Type:Journal Article
- Keywords:
autophagy;
chloroquine;
ethanol;
liver injury;
mouse
- MeSH:
Alanine Transaminase;
blood;
Animals;
Aspartate Aminotransferases;
blood;
Autophagy;
drug effects;
Chloroquine;
pharmacology;
Interleukin-6;
analysis;
Liver;
drug effects;
Liver Diseases, Alcoholic;
drug therapy;
Male;
Mice;
Mice, Inbred C57BL;
Microtubule-Associated Proteins;
metabolism;
Random Allocation;
Transcription Factor RelA;
metabolism;
Triglycerides;
analysis;
Tumor Necrosis Factor-alpha;
analysis
- From:
Chinese Journal of Applied Physiology
2018;34(2):102-105
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To investigate the role of autophagy inhibitor chloroquine (CQ) in acute ethanol-induced liver injury and its mechenism.
METHODS:Twenty-one C57BL/6 male mice were randomly divided into three groups:control group, ethanol group, CQ + ethanol group (=7). Mice in ethanol group were administered 33% (v/v) ethanol at a dose of 4.5 g/kg body weight. Ethanol-induced liver steatosis in each group was detected by hematoxylin and eosin staining. Hepatic lipid accumulation was detected by staining with Oil red O. Hepatic tissue triglyceride (TG) levels, serum aspartate aminotransferase(AST) and alanine aminotransferase(ALT) were determined by biochemical assays. Protein expression of microtubule-associated protein 1 light chain 3(LC3) and nuclear factorκB p65(NF-κB p65) were measured by Western blot and immunofluorescence. Pro-inflammatory factors tumor necrosis factor-α(TNF-α)、interleukin 6(IL-6) were detected by ELISA.
RESULTS:Compared with control group, ethanol induced liver injury proved by accumulation of hepatic lipids, TG levels, AST and ALT activities were significantly increased by ethanol, protein expression of LC3-Ⅱ was also markedly increased by ethanol. Compared with ethanol group, addition of CQ increased furtherthe level of LC3-Ⅱexpression, and TG amount, serum AST and ALT activities, and the expression of NF-κB p65, TNF-αand IL-6.
CONCLUSIONS:Acute ethanol-intake could induce liver steatosis and inflammation, and autophagy inhibitor CQ exacerbatedethanol-induced liver injury, suggested that autophagy might be protective effect in acute ethanol-induced liver disease.