20（S）-人参皂苷Rg3对脑缺血大鼠脑线粒体损伤的保护作用

Aim To study the mitochondria-protective effects of 20 (S)-ginsenoside Rg3 on focal cerebral ischemia injuries and its mechanism in rats. Methods Middle cerebral artery occlusion (MCAO) was used to induce focal cerebral ischemia model. After 24 h occlusion, cortex mitochondria was isolated and prepared for the measurement of membrane fluidity, swelling, phospholipid content, respiratory function, activities of mitochondrial respiratory enzymes and superoxide dismutase (SOD), contents of phospholipid, malondial dehyde (MDA) and Ca(superscript 2+) to evaluate the function of mitochondrial. Results Focal cerebral ischemia resulted in severe neuronal mitochondrial injuries, which could be alleviated by iv 20 (S)-ginsenoside Rg3 5 mg•kg^(-1), l0mg •kg^(-1), and nimodipine l.0mg•kg^(-1). The swelling of mitochondria was ameliorated, the decomposability of membrane phospholipid was decreased, the membrane fluidity of mitochondria was increased. 20 (S)-ginsenoside Rg3 also significantly inhibited the decrease in the activities of respiratory enzymes and SOD of mitochondrial, and the increase in MDA and Ca Ca(superscript 2+) levels caused by cerebral ischemia in rats. Conclusion 20 (S)-ginsenoside Rg3 showed a protective action against the cortex mitochondrial injuries in rats induced by cerebral ischemia. The mechanisms may be derived from reducing lipid peroxides, inhibiting Ca(superscript 2+) overload, scavenging free radicals and improving the energy metabolism.