Protective effect of asiatic acid from Potentilla chinensis on alcohol hepatic injury in rats.
- Author:
Gan ZHAO
;
Shu-juan LV
;
Gang WEI
;
Jin-bin WEI
;
Xing LIN
;
Quan-fang HUANG
- Publication Type:Journal Article
- MeSH:
Animals;
Liver;
drug effects;
pathology;
Liver Diseases, Alcoholic;
prevention & control;
Male;
NF-kappa B;
physiology;
Pentacyclic Triterpenes;
pharmacology;
Potentilla;
chemistry;
Protective Agents;
pharmacology;
Rats;
Rats, Wistar;
Toll-Like Receptor 4;
antagonists & inhibitors
- From:
China Journal of Chinese Materia Medica
2015;40(14):2866-2870
- CountryChina
- Language:Chinese
-
Abstract:
To study the protective effect and the mechanism of asiatic acid (AA) from Potentilla chinensis on alcohol hepatic injury in rats. Male Wistar rats were randomly divided into six groups: the normal control group, the AA control group (8 mg · kg(-1) AA), the model group (5.0-9.0 g · kg(-1) alcohol) and high, medium and low-dose AA-treated groups (alcohol + 8, 4, 2 mg · kg(-1) AA). Each group was orally administered with the corresponding drugs once a day for 24 weeks. Approximately 1. 5 hours after the final administration, all rats were killed, and their blood samples and hepatic tissues were collected. The AST and ALT in rat serum and the contents of MPO, TNF-α, IL-1β, SOD, GSH-Px, GSH-Rd and MDA in hepatic tissues were detected. The expressions of NF-κB, TLR4, CD14, MyD88, TRIF and protein expression in hepatic tissues were measured by western blot. The pathological changes in liver tissues were observed by histological examination. The results showed that compared with the model group, the AA-treated groups showed significant decreases in serum ALT, AST and MDA and increases in the activities of SOD, GSH-Px, GSH-Rd and MPO. Moreover, AA markedly inhibited the expressions of TNF-α, IL-1β, TLR4, CD14, MyD88 and NF-κB. The histological examination showed alleviated hepatic issue ijury to varying degrees. In short, asiatic acid (AA) from P. chinensis could protect alcohol-induced hepatic injury in rats. Its mechanism may be related to the inhibition of NF-κB inactivation and the reduction of inflammatory response.
