人参皂苷Rb_3对脑缺血大鼠脑线粒体损伤的保护作用

Protective effect of ginsenoside Rb_3 from rat cortex mitochondrial injuries due to cerebral ischemia

目的:研究人参皂苷Rb3对脑缺血大鼠脑线粒体损伤的保护作用,探讨人参皂苷Rb3抗缺血性脑中风的机制。方法:用栓线法制作大鼠大脑中动脉缺血(MCAO)模型,测定线粒体肿胀度、膜流动性、膜磷脂含量、呼吸功能、线粒体呼吸酶、超氧化物歧化酶(SOD)、丙二醛(MDA)和Ca2+等。结果:大鼠MCAO后24 h,脑线粒体损伤明显,表现为肿胀、膜流动性降低,膜磷脂降解、呼吸功能衰减,呼吸酶和SOD活性降低,Ca2+和MDA含量升高;静脉注射人参皂苷Rb3(5,10 mg·kg-1)能明显抑制缺血脑线拉体膜流动性的降低和膜磷脂的降解,减少脑缺血引起的线粒体肿胀,抑制NADH脱氢酶、琥珀酸脱氢酶和细胞色素C氧化酶活性的降低,改善线粒体呼吸功能;明显降低脑缺血大鼠脑神经细胞线粒体MDA含量,升高SOD活性,抑制Ca2+过多摄入。结论:人参皂苷Rb3对缺血脑神经细胞线粒体的损伤有明显的保护作用,该作用可能与清除氧自由基、抑制脂质过氧化、拮抗Ca2+有关。

Objective ：To assess the effect and mechanism of ginsenoside Rb3 in the protection of cerebral mitochondria of rats from focal cerebral ischemia injury. Methods： Rats were intravenously infused with ginsenoside Rb3（5 and 10 mg.kg^-1）. Subsequently, a focal cerebral ischemia model of the rats was set up by a middle cerebral artery occlusion （MCAO） technique. In 24 hours post the MCAO, the rats were euthanatized to collect the cortex mitochondria for the evaluation of membrane fluidity, mitochondrial swelling, phospholipid concentration, mitochondrial respiratory function, activities of mitochondrial respiratory enzymes and superoxide dismutase （SOD） , levels of phospholipid, malondial dehydride （MDA） and calcium ion. Results： Ginsenoside Rb3 alleviated the neuronal mitochondrial injuries and the mitochondrial swelling due to focal cerebral ischemia, and decreased the decomposability of membrane phospholipid and the membrane fluidity of mitochondria. Ginsenoside Rb3 significantly inhibited the decrease in the activities of respiratory enzymes and SOD of mitochondrial, and the increase in MDA and Ca^2＋ levels due to the focal cerebral ischemia. Conclusion：Ginsenoside Rb3 protected the cortex mitochondrial from impairment due to the cerebral ischemia by inhibiting lipid peroxides and Ca^2＋ overload and scavenging oxygen free radicals.