摘要
目的:探讨脑缺血耐受机制及清热化瘀方作为预处理药物对大鼠局灶性脑缺血再灌注损伤的保护作用。方法:采用线栓法制备大鼠大脑中动脉脑缺血预处理模型和再灌注模型。取健康雄性SD大鼠40只,随机分为假手术组、单纯脑缺血再灌注组、脑缺血预处理组、药物预处理组。再灌注后以免疫组化法测定Fas/FasL蛋白表达,TUNEL法检测细胞凋亡。结果:药物预处理能够抑制梗死后Fas/FasL表达(P<0.05),其作用程度与缺血预处理接近;药物预处理能抑制缺血半暗区神经元凋亡(P<0.05),其作用程度与缺血预处理相当。结论:脑缺血预处理可能通过抑制促凋亡蛋白Fas/FasL的合成发挥其神经保护作用,Fas/FasL是脑缺血耐受机制之一;清热化瘀方通过下调脑缺血后Fas/FasL的表达而减轻再缺血后神经元凋亡。
Objective ： To investigate the mechanism of ischemic tolerance and preconditioning effects of Qingre Huayu Prescription Extract（QRHYE） on the cerebral ischemia--reperfusion（CIR） injury in rats.Methods： CIR and ischemic preconditioning model were prepared by middle cerebral artery occlusion（MCAO） method in rats. Then,g0 animals were randomly divided into the sham operation group, cerebral ischemia--reperfusion injury group（IR）, cerebral ischemic preconditioning group（IPC） and QRHYE preconditioning group（QPC）.After reperfusion or preconditioning, the expression of Fas/FasL protein were detected by immunochemistry method and the number of apoptosis neuron in the penumbra region were observed by TUNEL method.Results ： （1）Both IPC and QPC had the same effect on inhabiting the expression of Fas/FasL protein （ P〈0.05 ） ; （2） Both IPC and QPC had the same effect on inhabiting neuronal apoptosis in the penumbra region （ P〈0.05 ）. Conclusions ： IP might protect neuron from ischemic injury by inhabiting the expression of pro-apoptosis protein Fas/FasL which was one of the mechanism of ischemlc tolerance. QRHYE could decrease neuronal apoptosis through downregulating the expression of Fas/FasL protein after reischemia in rats.
出处
《辽宁中医药大学学报》
CAS
2008年第8期153-154,共2页
Journal of Liaoning University of Traditional Chinese Medicine
