Keywords: 
• Lishukang capsule /
• high altitude hypoxia /
• brain tissue /
• protective effect

Abstract: Objective To investigate anti-hypoxia activity and protective effects of Lishukang capsule on rat brain tissue at simulated high altitude hypoxia. Methods The anti-hypoxic activity of Lishukang capsule was evaluated with normobaric hypoxia test and acute hypobaric hypoxia test in mice. In addition, rats were exposed to large hypobaric hypoxia chamber stimulating 8 000 m altitude. The pathological changes of rat brain tissue before and after hypoxia were observed. The oxidative stress indicators and metabolism parameters in brain were measured. Results The low, medium and high Lishukang doses can effectively prolong the survival time of mice (P<0.01) in the dose dependent manner. The medium and high Lishukang doses were significantly better than those of Rhodiola rosea capsules (P<0.05 or P<0.01). The low, medium, high Lishukang dose groups reduced the mortality of acute hypobaric hypoxia mice (P<0.01) with dose dependent effects. The mice mortality in medium and high dose groups was lower than that of Rhodiola rosea group (P<0.01). Compared with normal control group, the hypoxic model rats exhibited pathological injury in the brain tissue after exposure to hypobaric hypoxia stimulating 8 000 m altitude. The contents of MDA, H₂O₂, NO, LD and LDH activity increased significantly (P<0.05 or P<0.01), while the activities of SOD, CAT, GPX were significantly decreased (P<0.05 or P<0.01). After pretreatment with Lishukang capsule, the pathological damage of rat brain tissue was alleviated and the content of MDA, NO in the brain tissue was reduced (P<0.05 or P<0.01). The levels of H₂O₂, LD content and LDH activity in medium and high dose groups were significantly decreased (P<0.05 or P<0.01). The activities of SOD, CAT and GPX in high dose group were significantly increased (P<0.05). Conclusion Lishukang capsule has good anti-hypoxia activity. It provides protective effect for the injuries induced by hypobaric hypoxia in rats. The mechanism may related to the improvement of antioxidant capability, reduction of free radical damage and amelioration of energy metabolism.