Protective effect of the polysaccharide from Balanophora involucrata HK.f on liver injury induced by D-galactose in rats and its mechanism

Abstract

Objective: To investigate the protective effects and mechanisms of the polysaccharide from Balanophora involucrata HK.f (BIH) on liver injury induced by D-galactose in rats. Methods: Sixty male SD rats were randomly divided into 5 groups: the control group (n=12), the D-gal group (n=12), the BIH-L treatment group (D-gal+50 mg/kg BIH, n=12), the BIH-M treatment group (D-gal+100 mg/kg BIH, n=12), and the BIH-H treatment group (D-gal+200 mg/kg BIH, n=12). The rats were injected into the back of the neck with D-gal of 100 mg/kg/d subcutaneously except for the control group. The BIH treatment group were divided into BIH-L group (50 mg/(kg·d)), BIH-M group (100 mg/(kg·d)), and BIH-H group (200 mg/(kg·d)), respectively. The rats in the BIH group were intragastrically administrated with the relative BIH solution, while the rats in the control and D-gal group were treated with saline solution for 42 days. The serum contents of ALT, AST and DBIL c were tested by automatic biochemical analyzer, the content of MDA was determined by thiobarbital acid method and the SOD activity was detected by xanthine oxidase method. Expressions of Caspase-3, Bax, and Bcl-2 in liver were measured by Western blot, and morphological changes by HE staining and immunohistochemistry. Results: The serum contents of ALT, AST and DBIL in the D-gal group were significantly increased compared with those in Con group (P＜0.01) and were decreased in the BIH group as compared with the D-gal group (P＜0.01). Cell apoptosis, the Caspase-3 and Bax levels, and the MDA content in the D-gal group were increased compared with those in the control group (P＜0.01). And BIH treatment could attenuate these effects induced by D-gal. Meanwhile, the Bcl-2 level and SOD activity in the BIH group were increased compared with that in the D-gal group (P＜0.05, 0.01). Conclusion: BIH can protective liver injury through reducing cell apoptosis and inhibiting oxidative stress.