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目的:研究Fas/Fas L系统在缺血再灌注损伤人心脏微血管内皮细胞(HCMEC)凋亡通路中的作用,以及黄芪多糖(APS)对其干预作用,为APS更广泛的临床应用提供试验依据。方法:培养原代人心脏微血管内皮细胞,建立缺氧再灌注损伤模型,继而采用APS进行干预,随机分为:HCMEC正常对照组(control),HCMEC损伤组(HR),HCMEC损伤组+低浓度的药物(APS-L);HCMEC损伤组+中浓度的药物(APS-M),HCMEC损伤组+高浓度的药物(APS-H)。进而采用Western Blot、PCR等方法检测凋亡相关通路调控基因蛋白Fas、Fas L。结果:缺血再灌注损伤后基因蛋白Fas、Fas L表达显著上调(P<0.05),说明Fas、Fas L表达的增加与人心脏微血管内皮细胞凋亡增加呈平行关系;用APS治疗后Fas、Fas L表达减弱,随着APS浓度的升高,Fas及Fas L的表达逐渐减少,其中,中高剂量APS效果更明显(P<0.05)。结论:APS在一定程度上可抑制心肌缺血再灌注损伤中微血管内皮细胞凋亡,其机制可能与Fas/Fas L系统参与有关。
AIM: To investigate the role of Fas / Fas L system in the apoptotic pathway of human cardiac microvascular endothelial cells (HCMEC) induced by ischemia-reperfusion, and the intervention effect of APS, so as to provide experimental basis for the wider clinical application of APS . Methods: Primary human cardiac microvascular endothelial cells were cultured and hypoxia-reperfusion injury models were established. Then APS was used to intervene and randomly divided into three groups: HCMEC control group, HCMEC injury group, HCMEC injury group and low concentration (APS-L), HCMEC injury group + medium concentration drug (APS-M), HCMEC injury group + high concentration drug (APS-H). Then Western Blot, PCR and other methods to detect apoptosis-related pathway regulatory gene protein Fas, FasL. Results: The expressions of Fas and Fas L were significantly increased after ischemia-reperfusion (P <0.05), indicating that the increased expression of Fas and Fas L had a parallel relationship with the increase of apoptosis of human cardiac microvascular endothelial cells. After treated with APS, The expression of Fas L decreased, and the expression of Fas and Fas L gradually decreased with the increase of APS concentration. The effect of medium and high doses of APS was more obvious (P <0.05). Conclusion: APS can inhibit the apoptosis of microvascular endothelial cells in myocardial ischemia-reperfusion injury to a certain extent. The mechanism may be related to the involvement of Fas / Fas L system.