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目的:观察红景天苷(salidroside,Sal)对老龄大鼠局灶性脑缺血再灌注损伤的保护作用并探讨其作用机制。方法:采用线栓法制备老龄大鼠局灶性脑缺血再灌注损伤模型,观察红景天苷对老龄大鼠局灶性脑缺血再灌注后神经功能障碍,脑水肿及脑梗死范围以及对脑缺血2h再灌注24h缺血脑组织能量物质ATP、葡萄糖无氧酵解产物以及体内自由基清除剂SOD、GSH和脂质过氧化产物MDA等生化物质的影响。结果:脑缺血2h再灌注24h腹腔注射Sal40,20,10mg.kg-1可明显减轻神经功能障碍(P<0.05,P<0.01),减轻脑水肿(P<0.05,P<0.01)及缩小脑梗死范围(P<0.05)。同时Sal40,20,10mg.kg-1组与缺血再灌注组相比,缺血脑组织内SOD活性和GSH活力明显增高(P<0.05,P<0.01),MDA含量显著降低(P<0.05,P<0.01),大鼠脑组织内ATP含量显著升高(P<0.05,P<0.01),脑组织内LA含量明显降低(P<0.05,P<0.01)。结论:红景天苷对老龄大鼠局灶性脑缺血再灌注损伤有良好的保护作用。其机制与其改善缺血脑组织能量代谢、降低自由基损伤有关。
Objective: To observe the protective effect of salidroside (Sal) on focal cerebral ischemia-reperfusion injury in aged rats and to explore its mechanism. Methods: The model of focal cerebral ischemia-reperfusion injury in aged rats was established by thread-plug method. The effects of salidroside on neurological deficits, cerebral edema and cerebral infarction after focal cerebral ischemia-reperfusion in aged rats were observed. On cerebral ischemia 24h reperfusion 24h ischemic brain energy substances ATP, glucose anaerobic glycolysis products and free radical scavengers in vivo SOD, GSH and lipid peroxidation product MDA and other biochemical substances. Results: Intraperitoneal injection of Sal40, 20 and 10 mg.kg-1 at 2 h reperfusion 24h after cerebral ischemia could significantly reduce neurological dysfunction (P <0.05, P <0.01), alleviate cerebral edema (P <0.05, P <0.01) Range of cerebral infarction (P <0.05). Compared with ischemia reperfusion group, the activity of SOD and the activity of GSH in Sal40,20,10mg.kg-1 group were significantly increased (P <0.05, P <0.01) , P <0.01). The content of ATP in brain tissue of rats increased significantly (P <0.05, P <0.01), and the content of LA in brain tissue decreased significantly (P <0.05, P <0.01). Conclusion: Salidroside has a good protective effect on focal cerebral ischemia-reperfusion injury in aged rats. Its mechanism and its improvement of ischemic brain energy metabolism, reduce free radical damage related.