论文部分内容阅读
目的:探讨补肾醒脑方有效部位对大脑局灶性脑缺血后再灌注大鼠脑组织白细胞介素-1β(IL-1β)和细胞间黏附分子-1(ICAM-1)表达的作用。方法:采用大鼠大脑中动脉闭塞局灶性脑缺血再灌注模型,观察补肾醒脑方有效部位对脑缺血大鼠神经功能的影响,用免疫组化法检测脑组织IL-1β和ICAM-1的表达。结果:脑缺血2 h再灌注46 h后,模型组与假手术组比较海马及髓质区IL-1β表达阳性细胞数显著增加(P<0.05,P<0.01),海马及皮质区ICAM-1表达阳性细胞数显著增多(P<0.01,P<0.05);补肾醒脑方有效部位生物碱可使髓质区IL-1β阳性细胞数显著减少(P<0.01);苷可使皮质区ICAM-1β阳性细胞数显著减少(P<0.01)。结论:脑缺血再灌注后,脑组织IL-1β和ICAM-1表达增加,补肾醒脑方有效部位能明显改善因缺血所致神经行为功能缺失,生物碱和苷可分别抑制髓质部位IL-1β蛋白表达及皮质区ICAM-1蛋白表达,提示生物碱和苷可能是补肾醒脑方抗脑缺血后炎症反应的部分物质基础。
Objective: To investigate the effects of Bushen Xingnao Decoction on the expression of interleukin-1β (IL-1β) and intercellular adhesion molecule-1 (ICAM-1) in brain tissue after focal cerebral ischemia / reperfusion in rats. Methods: The focal cerebral ischemia-reperfusion model of rats with middle cerebral artery occlusion was used to observe the effects of Bushen xingnao recipe on neurological function in rats with cerebral ischemia. Immunohistochemistry was used to detect the expression of IL-1β and ICAM -1 expression. Results: The number of IL-1β-positive cells in the hippocampus and medulla increased significantly (P <0.05, P <0.01) in hippocampus and cortex at 46 h after reperfusion at 2 h after cerebral ischemia. ICAM- (P <0.01, P <0.05). The alkaloids in Bushen Xingnao Prescription could decrease the number of IL-1β positive cells in the medulla (P <0.01) -1β-positive cells decreased significantly (P <0.01). Conclusion: After cerebral ischemia-reperfusion, the expression of IL-1β and ICAM-1 in brain tissue increased. The effective site of Bushen xingnao can obviously improve the neurobehavioral deficit caused by ischemia. Alkaloid and glycoside can inhibit the medulla site IL-1βprotein expression and cortex ICAM-1protein expression, suggesting alkaloids and glycosides may be Bushenxingnao anti-cerebral ischemia part of the material basis of inflammation.