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目的:观察麝香酮对过氧化氢(H2O2)诱导人血管内皮细胞(HUVEC)凋亡的保护效应,并探讨其作用机制。方法:运用H2O2建立血管内皮细胞凋亡模型,继而用低、中、高不同剂量的麝香酮进行干预,并用MTT法检测细胞增殖,Hoechst 33258荧光染色及流式细胞技术检测细胞凋亡,激光共聚焦显微镜测定Ca2+浓度和线粒体膜电位(ΔΨm)的变化。结果:H2O2诱导HUVEC细胞凋亡,中、高剂量的麝香酮对HUVEC细胞增殖均有明显促进作用;H2O2组与正常组相比ΔΨm显著下降,Ca2+浓度明显升高(P<0.01);中、高剂量组与H2O2组相比ΔΨm则显著升高,Ca2+浓度明显降低(P<0.01)。结论:麝香酮可通过稳定线粒体ΔΨm,减轻细胞通透性,减少Ca2+内流,从而抑制H2O2所致的HUVEC细胞凋亡。
Objective: To observe the protective effect of musk ketone on the apoptosis of human vascular endothelial cells (HUVEC) induced by hydrogen peroxide (H2O2) and to explore its mechanism. Methods: Apoptosis model of vascular endothelial cells was established by H2O2, followed by intervention with low, medium and high doses of musk ketone. Cell proliferation was detected by MTT assay. Cell apoptosis was detected by Hoechst 33258 staining and flow cytometry. Changes of Ca2 + concentration and mitochondrial membrane potential (ΔΨm) were measured by focusing microscope. Results: H2O2 induced the apoptosis of HUVEC cells, and moderate and high doses of musk ketone promoted the proliferation of HUVECs significantly. Compared with the normal group, ΔΨm decreased significantly and the concentration of Ca2 + increased significantly (P <0.01) Compared with H2O2 group, ΔΨm increased significantly and Ca2 + concentration decreased significantly in high dose group (P <0.01). CONCLUSION: Musk ketone can inhibit H2O2-induced HUVEC apoptosis by stabilizing mitochondrial ΔΨm, reducing cell permeability and decreasing Ca2 + influx.