白藜芦醇苷对羟自由基所致大鼠脑线粒体氧化损伤的保护作用

目的　研究白藜芦醇苷对氧自由基所致大鼠脑线粒体损伤的保护作用 ,探讨白藜芦醇苷治疗心脑血管疾病的机制。方法　利用Fe2 + +VitC系统产生·OH ,诱导大鼠脑线粒体损伤 ;测定线粒体肿胀度、膜流动性、膜磷脂含量以显示线粒体膜功能 ,测定ATPase ,细胞色素C氧化酶活性以显示线粒体能量代谢能力 ,测定超氧化物歧化酶 (SOD)、丙二醛(MDA)以显示线粒体抗氧化能力。结果　·OH造成线粒体显著损伤 ,白藜芦醇苷 (终浓度 10 0、2 0 0、4 0 0mg·L-1)明显抑制膜磷脂降解、线粒体肿胀 ,增加膜流动性 ,改善线粒体能量代谢状态 ,增强抗氧化能力。结论　白藜芦醇苷对氧自由基所致大鼠脑线粒体损伤有明显保护作用 ,其机制与清除自由基、抑制脂质过氧化有关

Protective effect of Polydatin against rat cortex mitochondria injury induced by·OH

AIM To study the effects of polydatin on free radical induced rat cortex mitochondria injury. METHODS Fe 2++VitC system was used to produce ·OH. The mitochondria was isolated. Mitochondria membrane fluidity, swelling and contents of phospholipid were determined to measure the function of mitochondria membrane. The activities of ATPase and Cytochrome C oxidase were determined to measure the ability of mitochondria energy metabolism. The activity of superoxide dismutase (SOD) and content of malondial dehyde (MDA) were determined to measure the ability of anti oxygenation. RESULTS ·OH resulted in severe neuronal mitochondria injuries and the injuries and the injuries was alleviated by Polydatin (content of 100,200,400 mg·L -1). The swelling of mitochondria was ameliorated, the decomposability of mitochondrion membrane phospholipid was decreased, the membrane fluidity of mitochondria was increased. Polydatin also significantly inhibited the decrease in SOD, Cytochrome C oxidase and ATPase activity and the increase in MDA levels caused by free radical. CONCLUSION Polydatin has a protective action against the rat neuronal mitochondria injuries induced by oxygen free radical. The mechanisms may be derived from scavenging free radicals, reducing lipid peroxides, and improving the energy metabolism.