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目的:研究银杏叶制剂对大鼠脑缺血再灌注后热休克蛋白(HSP)、C-FOS表达的影响,探讨其神经保护机制。方法:采用改良LONGA法复制大鼠局灶脑缺血再灌注模型。56只实验大鼠随机分为正常对照组、假手术组、缺血再灌注组及银杏叶制剂预处理组。银杏组大鼠在实验前灌服银杏制剂2 ML,1日3次,连用5 D。应用HSP70及 C-FOS免疫组化染色、C-FOS MRNA原位杂交、原位细胞凋亡及HE染色等方法观察缺血再灌注不同时点(1 H、6 H、12 H、24 H、3 D、7 D)两者的变化,并对其阳性结果进行半定量分析。结果:银杏制剂预处理组各时段神经细胞缺血程度明显轻于未处理组、TUNEL阳性细胞数明显少于未处理组,HSP70及C-FOS表达的阳性细胞数则明显多于未处理组 (P<0．01)。脑缺血再灌注组1 H时C-FOS即有表达,6 H达高峰,后逐渐下降。再灌注6 H组HSPT0在缺血侧皮质及基底节开始表达,24 H达高峰。再灌注6 H细胞凋亡最显著。结论:银杏制剂可能通过诱导HSP70及C-FOS的表达, 发挥其神经保护作用。
Objective: To study the effects of Ginkgo biloba extract on the expression of heat shock protein (HSP) and C-FOS after cerebral ischemia-reperfusion in rats and to explore its neuroprotective mechanism. Methods: The rat model of focal cerebral ischemia and reperfusion was duplicated by modified LONGA method. 56 experimental rats were randomly divided into normal control group, sham operation group, ischemia-reperfusion group and ginkgo leaf pretreatment group. The ginkgo group rats were given 2 g of Ginkgo biloba before the experiment, three times a day, and 5 D were used. HSP70 and C-FOS immunohistochemical staining, C-FOS MRNA in situ hybridization, in situ cell apoptosis and HE staining were used to observe ischemia reperfusion at different time points (1 H, 6 H, 12 H, 24 H, 3 D, 7 D) Changes in both, and semi-quantitative analysis of positive results. RESULTS: The degree of nerve cell ischemia was significantly lighter than that of the untreated group and the number of TUNEL-positive cells in the Ginkgo biloba pretreatment group was significantly lower than that in the untreated group. The number of HSP70 and C-FOS positive cells was significantly higher than that of the untreated group ( P<0.01). In cerebral ischemia-reperfusion group, C-FOS was expressed at 1 H, peaked at 6 H, and then gradually decreased. Reperfusion of 6H group HSPT0 began in the cortex and basal ganglia of the ischemic side and reached a peak at 24 H. Apoptosis was most pronounced in reperfusion 6 H cells. CONCLUSION: Ginkgo biloba may exert its neuroprotective effect through induction of HSP70 and C-FOS expression.