猕猴脑动脉硬化自由基损伤机制

Damage mechanism of free radical in experimental cerebral arteriosclerosis in rhesus monkey

目的 :研究脑动脉硬化与自由基损伤关系。方法 :2 5只健康猕猴 ,其中 6只成年猴、3只老年猴饲以含 1%胆固醇的混合高脂饲料 16mon～ 2 8mon ,13只成年猴和 3只老年猴作对照 ,测定血浆和动脉壁胆固醇、MDA、SOD ,扫描电镜和透射电镜观察大脑中动脉及中央支损害。结果 :模型组脑动脉壁总胆固醇每 5 0mg湿重为 1 10 9±0 0 2 9mg ,MDA每 10 0mg湿重组织 1 918± 0 330mol,SOD每 10 0mg湿重组织 180 715 9u ,明显高于对照组 (总胆固醇0 0 5 5± 0 0 2 7mg ,MDA0 2 88± 0 370nmol,SOD6 14± 6 7 5u)。模型组大脑中动脉内皮水肿 ,表面胞浆突起增多 ,微绒毛消失 ,局部内皮破裂 ,血细胞、血小板粘附。随造型时间延长 ,病损加重。老年猴中央支也呈现出较严重的动脉硬化改变。结论 :高脂血症可导致脂质过氧化 。

Objective: To study the relationship between the cerebral arteriosclerosis and the damage of free radical.Methods: Twenty_five healthy rhesus monkeys, six adult and three old monkeys were fed with standard monkey pellets with 1% cholesterol for 16mon～28mon, thirteen adult and three old ones served as the control group, cholesterol, MDA, SOD in the plasma and cerebral artery were tested, the changes of middle cerebral artery and its central branches were observed by SEM and TEM, Result: The total cholesterol value of cerebral wall in the model group (1 109±0 029 VS 0 055±0 027mg/50mg wet weight), MDA(1 918±0 330 VS 0 288±0 370nmol/100mg wet weight) and SOD (180 7±159 6 VS 614 0±67 5u/100mg wet weight) were sign ficantly different from those in the control groups. In the model group, there was edema in the endothelium of middle cerebral artery, more cytoplasm projecting on the surface, microvilli disapeared, some endothelial cells were disruptured, and blood cells and platelets adhered. As the time prolonged, the damage of artery was worse. The central branches appeared severe degees of arteriosclerosis in the old experimental group. Conclusion: Hyperlipidemia can induce lipid peroxidation and the damage of free radical may play a role in the lesion development of cerebral arteriosderosis.