Abstract:

BACKGROUND: Epidemiologic survey demonstrated that high-altitude hypoxia may result in liver injury, but there are few studies relate to the pathogenesis. Salidroside, the main active component of Gold Theragran, has been showed effects on removing oxygen free radical and protecting cell membrane.
OBJECTIVE: To observe the protective effect of salidroside on rat’s liver injury caused by imitating altitude liver hypoxia with hepatic artery ligation.
METHODS: Wistar rats were randomly divided into 3 groups: ligation group, salidroside + ligation group and normal control group. Rats in the former two groups were prepared for hepatic artery ligation models and divided into five time sections as 1, 2, 4, 6, 8 hours. In the salidroside + ligation group, rats were intraperitoneal injected salidroside solution at 2 days, 1 day and 2 hours prior to ligation. Liver function targets in serum were detected by automatic biochemistry analyzer; the content of malonaldehyde was detected by thiobarbituric acid method; the activity of superoxide dismutase (SOD) was detected with xanthine oxidase method; pathological changes in liver tissue were observed by hematoxylin-eosin staining; the level of hypoxia-inducible factor 1α (HIF-1α) protein was detected with immunohistochemistry; and apoptosis in liver tissue was detected by TUNEL method.
RESULTS AND CONCLUSION: Imitating altitude liver hypoxia by hepatic artery ligation could cause liver’s acute injury. Intervention with salidroside could improve rat’s liver function targets (P < 0.05), lower the content of malonaldehyde and heighten the activity of SOD (P < 0.05), abate liver tissue’s histopathological change, increase HIF-1α protein level (P < 0.05), and lessen cell apoptosis in liver tissues (P < 0.05). Salidroside have protective effect on rat’s acute liver injury induced by imitating altitude liver hypoxia with hepatic artery ligation by opposing oxidative stress and inhibiting cell apoptosis.