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目的观察他克莫司(FK506)对缺氧培养条件下人脐静脉血内皮细胞(HuVECs)凋亡的作用及其可能机制。方法将HuVECs细胞分为四组:正常对照组(A组)、FK506干预组(B组)、缺氧组(C组)和缺氧条件下FK506干预组(D组)。应用细胞计数试剂盒-8(CCK-8)和Hoechst 33342染色分别检测细胞活性和凋亡;Western blot检测内质网应激相关蛋白的表达。结果与A组相比,D组HuVECs凋亡率、内质网应激相关蛋白表达均明显增加(P<0.01或P<0.05)。结论 FK506促进了缺氧诱导的内皮细胞凋亡,从而抑制新生血管的发生。
Objective To investigate the effect of FK506 on apoptosis of human umbilical vein endothelial cells (HuVECs) under hypoxia and its possible mechanism. Methods HuVECs were divided into four groups: normal control group (group A), FK506 intervention group (group B), hypoxia group (group C) and hypoxic condition FK506 intervention group (group D). Cell viability and apoptosis were detected by cell counting Kit-8 (CCK-8) and Hoechst 33342 staining, respectively. The expression of ER stress-related proteins was detected by Western blot. Results Compared with group A, the apoptotic rate of HuVECs and the expression of stress related proteins in endoplasmic reticulum in group D were significantly increased (P <0.01 or P <0.05). Conclusion FK506 promotes hypoxia-induced endothelial cell apoptosis and thus inhibits neovascularization.