Abstract: Objective To study the effects of Balanophora polysaccharides (BPS) on the expression of BDNF, TrkB and other apoptosis-related proteins in rats with experimental liver injury induced by D-gal. Methods Rats were randomly divided into control group, D-gal group (200 mg/kg of hypodermic D- galactose), groups with BPS of low dosage (BPS-L), medium dosage (BPS-M) and high dosage (BPS-H), which were treated with intragastric administration by 50, 100 and 200 mg/kg BPS per day, respectively. After six weeks, serum alanine transaminase(ALT) and aspartate aminotransferase(AST) were measured. HE staining was used to observe liver tissue morphology. The localization of BDNF and TrkB was determined by immuno-histochemical staining. Western blot was used to detect BDNF, TrkB, Bcl-2, caspase-3 and Bax protein expression. ELISA was used to determine the malondialdehyde(MDA) content and superoxide dismutase(SOD) activity in liver tissues. Results Compared with the control group, the hepatocytes showed edema and punctate necrosis in D-gal group, with increased serum level of ALT and AST(P＜0.05). The results also showed decreased SOD activity and increased MDA content (P＜0.05), increased Bax, caspase-3, BDNF, TrkB expression (P＜0.05) and decreased Bcl-2 expression (P＜0.05). Compared to D-gal group, the hepatocyte degeneration and necrosis were obviously alleviated in BPS groups with each dose accompanied by decreased serum ALT and AST levels (P＜0.05), increased SOD activity and decreased MDA content (P＜0.05), reduced Bax and caspase-3 expression of pro-apoptotic proteins, increased expression Bcl-2 anti-apoptotic proteins (P＜0.05) and decreased expression of BDNF and TrkB (P＜0.05). Conclusions Balanophora polysaccharide had a protective effect on experimental liver injury caused by D-gal. The mechanism may be related to the decrease of the expression of BDNF and TrkB followed by inhibition of hepatocyte apoptosis.

Key words: Balanophora polysaccharide, liver injury, apoptosis, BDNF/TrkB