The catalase inhibitor aminotriazole alleviates acute alcoholic liver injury.
- Author:
Qing AI
1
;
Pu GE
2
;
Jie DAI
3
;
Tian-Cai LIANG
2
;
Qing YANG
2
;
Ling LIN
2
;
Li ZHANG
4
Author Information
1. Department of Physiology, Chongqing Medical University, Chongqing 400016, China.
2. Department of Pathophysiology, Chongqing Medical University, Chongqing 400016, China.
3. Hospital of Chongqing University of Arts and Sciences, Chongqing 402160, China.
4. Department of Pathophysiology, Chongqing Medical University, Chongqing 400016, China. zhangli@cqmu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Alanine Transaminase;
metabolism;
Amitrole;
pharmacology;
Animals;
Aspartate Aminotransferases;
metabolism;
Catalase;
antagonists & inhibitors;
Ethanol;
Hydrogen Peroxide;
metabolism;
Interleukin-6;
blood;
L-Lactate Dehydrogenase;
metabolism;
Liver;
enzymology;
Liver Diseases, Alcoholic;
drug therapy;
Malondialdehyde;
metabolism;
Rats;
Rats, Sprague-Dawley;
Tumor Necrosis Factor-alpha;
blood
- From:
Acta Physiologica Sinica
2015;67(1):97-102
- CountryChina
- Language:Chinese
-
Abstract:
In this study, the effects of catalase (CAT) inhibitor aminotriazole (ATZ) on alcohol-induced acute liver injury were investigated to explore the potential roles of CAT in alcoholic liver injury. Acute liver injury was induced by intraperitoneal injection of alcohol in Sprague Dawley (SD) rats, and various doses of ATZ (100-400 mg/kg) or vehicle were administered intraperitoneally at 30 min before alcohol exposure. After 24 h of alcohol exposure, the levels of aspartate transaminase (AST), alanine transaminase (ALT) and lactate dehydrogenase (LDH) in plasma were determined. The degree of hepatic histopathological abnormality was observed by HE staining. The activity of hepatic CAT, hydrogen peroxide (H₂O₂) level and malondialdehyde (MDA) content in liver tissue were measured by corresponding kits. The levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in plasma were determined by ELISA method. The results showed that treatment with ATZ dose-dependently suppressed the elevation of ALT, AST and LDH levels induced by alcohol exposure, and that ATZ alleviated alcohol-induced histopathological alterations. Furthermore, ATZ inhibited the activity of CAT, reduced hepatic levels of H₂O₂and MDA in alcohol exposed rats. ATZ also decreased the levels of plasma TNF-α and IL-6 in rats with alcohol exposure. These results indicated that ATZ attenuated alcohol-induced acute liver injury in rats, suggesting that CAT might play important pathological roles in the pathogenesis of alcoholic liver injury.
