山莨菪碱对全脑缺血-再灌流后脑线粒体损伤的保护作用

The protective effects of anisodamine on brain mitochondria damage after complete cerebral ischemia and reperfusion in rabbits

目的 探讨山莨菪碱对急性全脑缺血 再灌流后脑线粒体损伤的保护作用。方法 采用家兔全脑缺血 再灌流损伤模型。缺血 2 0min ,再灌流 2h ,观察脑线粒体呼吸功能、呼吸链氧化酶活性、线粒体内Ca2 + 和丙二醛含量的变化。结果 脑缺血 再灌流后 ,脑线粒体呼吸控制率、磷氧化、氧化磷酸化效率及烟酰胺腺嘌呤二核苷酸氧化酶、琥珀酸氧化酶、细胞色素C氧化酶活性明显降低 (P <0 0 1) ,而线粒体Ca2 + 、丙二醛含量明显升高 (P <0 0 1) ;再灌流早期给予山莨菪碱治疗后 ,上述线粒体损伤性改变明显减轻。结论 山莨菪碱对脑缺血 再灌流后线粒体损伤具有一定的保护作用 ,其机制可能与Ca2 + 拮抗、抑制脂质过氧化及保护呼吸链酶活性有关。

Objective To explore the protective effects of anisodamine on brain mitochondria damage after complete cerebral and reperfusion in rabbits.Methods The rabbit model of acute complete cerebral ischemia and reperfusion were used.Ischemia for twenty minutes followed by reperfusion for two hours,the cortex mitochondrial respiratory function,activities of nicotinamide adenine dinucleotide(NADH) oxidase,succinate oxidase and cytochrome C oxidase in respiratory chain,contents of calciu,and malondiadhyde(MDA)in mitochondria were observed.Results In ischemia reperfusion group,the brain mitochondrial respiratory control rate(RCR),ADP/O ratio,oxidation phospharation rate(OPR),and the activities of above three oxidases reduced significantly( P <0 01),but the contents of mitochondrial Ca 2+ and MDA increased markedly,compared with those in sham group.After treated with anisodamine in early stage of reperfusion,the above brain mitochondria damages were attenuated significantly.Conclusion The results show that anisodamine protect brain mitochondia against damage induced by ischemia and reperfusion.The mechanism may be connected with antagonism of calcium,inhibition of lipid peroxide,and keeping activities of respiratory chain oxidases.