论文部分内容阅读
目的:通过对观察丹酚酸A预处理对局灶性脑缺血再灌注损伤大鼠ICAM-1表达的影响,探讨丹酚酸A预处理对缺血再灌注急性期脑损伤的保护作用机制。方法:丹酚酸A预处理3天后采用线拴法建立大鼠脑缺血再灌注模型,不同时间点(0,1,4,12,24h)取脑组织,冰冻切片,荧光免疫组化法检测缺血区脑微血管内皮ICAM-1的表达。以尼莫地平作为阳性对照药。结果:模型组与空白对照组相比ICAM-1表达明显升高(P<0.05)。丹酚酸A各组ICAM-1表达均低于相应时间点模型组(P<0.05)。结论:丹酚酸A预处理可降低局灶性脑缺血再灌注损伤大鼠ICAM-1表达的影响,提示阻抑粒细胞粘附作用是其脑保护作用机制之一。
OBJECTIVE: To investigate the protective effect of salvianolic acid A preconditioning on acute cerebral ischemia-reperfusion injury in rats by observing the effects of salvianolic acid A preconditioning on ICAM-1 expression in rats with focal cerebral ischemia-reperfusion injury. . METHODS: After 3 days of salvianolic acid A pretreatment, cerebral ischemia reperfusion model was established by the ray method. Brain tissues were taken at different time points (0, 1, 4, 12, 24h) and frozen sections were used. Fluorescence immunohistochemistry The expression of ICAM-1 in the cerebral microvascular endothelium in ischemic region was detected. Nimodipine was used as a positive control drug. Results: The expression of ICAM-1 in the model group was significantly higher than that in the control group (P<0.05). The expression of ICAM-1 in each group of salvianolic acid A was lower than that in the corresponding time point model group (P<0.05). CONCLUSION: Pretreatment with salvianolic acid A can reduce the expression of ICAM-1 in rats with focal cerebral ischemia-reperfusion injury, suggesting that inhibition of granulocyte adhesion is one of the mechanisms of brain protection.