心脑肾康对脑缺血的干预作用及机制探讨  

Effects of Xinnaoshenkang on cerebral ischmia injury of rats and its mechanism

作　　者：梁钢[1] 简洁[1] 藏林泉[2] 黄志明[1] 韦郑凯[1] 黄建春[3] 

机构地区：[1]广西医科大学药理学教研室,广西南宁530021 [2]中山大学医学院药理教研室,广东广州510080 [3]广西医科大学

出　　处：《中国药理学通报》2005年第8期959-961,共3页Chinese Pharmacological Bulletin

基　　金：广西科技厅科研基金资助项目(No桂科攻02350243号)

摘　　要：目的探讨心脑肾康对大鼠局灶性脑缺血-再灌注损伤的干预作用及可能机制。方法用线栓阻断大鼠大脑中动脉,制作局灶性脑缺血再灌注模型(MCAO模型),缺血1.5h再灌24h后腹主动脉采血,测定血小板聚集率;断头取脑,检测大脑皮层多项生化指标。结果心脑肾康口服能使脑缺血大鼠的神经行为明显改善,脑梗死面积降低;与模型组相比,高、中、低3个剂量组均能降低缺血后脑组织匀浆中的丙二醛(MDA)、乳酸(LA)、活性氧(ROS)、一氧化氮合酶(NOS)含量,提高超氧化物歧化酶(SOD)、ATPase活性(P<0.05),并具明显的抑制血小板聚集作用。结论心脑肾康对大鼠局灶性脑缺血有明显保护作用。Aim To study the protective effects of Xinnaoshenkang （XNSK） against focal cerebral injury caused by ischmia-reperfusion in rats and its mechanism. Methods The focal brain ischmia-reperfusion model in rats was made through by using an intralumihal monofilament to occlude the middle cerebral artery for 1.5 h and then reperfusing for 24h. Spectrophotometric assay was used to measure the contents of malondial-dehyde （ MDA）, lactic acid （ LA）, superoxide dismutase（SOD） , reactive oxygen species（ROS） , nitricoxide synthase （NOS） and several ATPase in cerebral cortex homogenates from rats. The effects on platelet aggregation were also observed. Results Compared with model and positive control groups,88,175, 350 mg·kg^-1 XNSK groups were found having significant inhibition of cerebral infarction, MDA, LA, ROS,NOS, platelet aggregation and significant increase of the activity of SOD, ATPase. Conclusion XNSK has protective effects against focal cerebral injury caused by ischmia-reperfusion in rats.

关 键 词：心脑肾康 脑缺血-再灌注损伤 干预 

分 类 号：R-332[医药卫生] R289