Schisandrin B attenuates acetaminophen-induced hepatic injury through heat-shock protein 27 and 70 in mice

• Published in: Journal of gastroenterology and hepatology 2014-03, Vol.29 (3), p.640-647
• Main Authors: Li, Libo, Zhang, Tiran, Zhou, Li, Xing, Guihua, Chen, Yuhang, Xin, Yabing
• Format: Article
• Language: English
• Subjects: acetaminophen; Acetaminophen - adverse effects; Administration, Oral; Animals; Chemical and Drug Induced Liver Injury - drug therapy; Chemical and Drug Induced Liver Injury - genetics; Chemical and Drug Induced Liver Injury - metabolism; Chemical and Drug Induced Liver Injury - prevention & control; Cyclooctanes - administration & dosage; Cyclooctanes - pharmacology; Cyclooctanes - therapeutic use; Disease Models, Animal; Dose-Response Relationship, Drug; Gene Expression - drug effects; heat-shock protein; HSP27 Heat-Shock Proteins - genetics; HSP27 Heat-Shock Proteins - metabolism; HSP70 Heat-Shock Proteins - genetics; HSP70 Heat-Shock Proteins - metabolism; Lignans - administration & dosage; Lignans - pharmacology; Lignans - therapeutic use; Liver - metabolism; liver injury; Male; Mice; Phytotherapy; Polycyclic Compounds - administration & dosage; Polycyclic Compounds - pharmacology; Polycyclic Compounds - therapeutic use; Schisandra; Schisandrin B; Time Factors
• ISSN: 0815-9319; 1440-1746
• DOI: 10.1111/jgh.12425

Background and Aim Schisandrin B is an active component isolated from Schisandra chinensis (TurcZ.) Baill. that is widely used as an antihepatotoxic agent. Schisandrin B has significant hepatoprotective effect against chemical and immunological liver injury. This study aimed to investigate the effect of Schisandrin B on the expression of 27‐ and 70‐kDa heat‐shock protein (HSP) and its role in protection against acetaminophen‐induced liver injury in mice. Methods After the mice were pretreated, Western blot and real‐time quantitative polymerase chain reaction were used to detect the protein and gene expression of HSP27 and HSP70, respectively; the liver tissues were subjected to histological evaluation, and alanine aminotransferase and aspartate aminotransferase activities in the serum were measured. Results Oral administration of Schisandrin B increased the expression of HSP27 and HSP70 in a time‐ and dose‐dependent manner. The inducing effect of Schisandrin B on HSP27 and HSP70 was also confirmed by real‐time quantitative polymerase chain reaction. In the acetaminophen‐induced liver injury mouse model, the prior oral administration of Schisandrin B (200 mg/kg) three times in 24 h markedly alleviated liver injury as indicated by the amelioration of histopathological hepatic necrosis and the reduction of alanine aminotransferase and aspartate aminotransferase activities in the serum. However, the earlier actions of Schisandrin B were all suppressed significantly by Quercetin, a known HSP inhibitor. Conclusion The hepatic cytoprotective action of Schisandrin B against acetaminophen‐induced liver injury is mediated, at least in part, by the induction of HSP27 and HSP70 in mice.