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目的:探讨地奥心血康对培养H9c2心肌细胞缺氧/复氧损伤的保护作用机制。方法:建立缺氧/复氧损伤心肌细胞模型,用地奥心血康进行干预。将培养的H9c2心肌细胞随机分为6组,正常对照组(C组);缺氧/复氧模型组(H/R组);缺氧/复氧模型+吡那地尔(pinacidil,Pin)阳性对照组(H/R+Pin组);缺氧/复氧模型+地奥心血康(DAXXK)低剂量、中、高剂量(10mg/L、20 mg/L、40mg/L)干预组(H/R+L、M、H组)。MTT法测定细胞存活率;用罗丹明123(Rh123)荧光探针标记线粒体,在荧光显微镜下采集被Rh123染色的各组心肌细胞荧光图片;收集培养细胞上清液测定乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)的活性及丙二醛(MDA)的含量。结果:与正常组比较,缺氧/复氧模型组细胞存活率、线粒体膜电位及SOD活性均下降,而LDH活性、MDA含量均升高。地奥心血康用药组可有效提高心肌细胞存活率、升高线粒体膜电位,同时降低受损心肌LDH的释放量,并有效提高SOD的活性,减少MDA的生成量。结论:地奥心血康对缺氧/复氧造成的H9c2心肌细胞损伤具有保护作用,其机制与保护细胞线粒体膜、增强细胞清除氧自由基能力、减少脂质过氧化物的产生有关。
Objective: To investigate the protective mechanism of Diorexinxuekang on hypoxia / reoxygenation injury in cultured H9c2 cardiomyocytes. Methods: To establish hypoxia / reoxygenation injury model of cardiomyocytes, with the intervention of Dioxinkangkang. The cultured H9c2 cardiomyocytes were randomly divided into 6 groups, normal control group (C group), hypoxia / reoxygenation model group (H / R group), hypoxia / reoxygenation model + pinacidil (Pin) (H / R + Pin group), hypoxia / reoxygenation model + DAXXK intervention group (H / R + 10 mg / L, 20 mg / L, 40 mg / L) + L, M, H group). Cell viability was measured by MTT assay. Mitochondria were labeled with Rh123 fluorescent probe. Fluorescent images of cardiomyocytes stained with Rh123 were collected under fluorescent microscope. Lactate dehydrogenase (LDH) , Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. Results: Compared with the normal group, the cell viability, mitochondrial membrane potential and SOD activity in hypoxia / reoxygenation model decreased, while the activities of LDH and MDA increased. Dioxintangxuankang could increase the survival rate of cardiomyocytes, increase the mitochondrial membrane potential, decrease the release of LDH in injured myocardium, increase the activity of SOD and decrease the production of MDA. CONCLUSION: DIA has a protective effect on H9c2 cardiomyocytes injury induced by anoxia / reoxygenation. Its mechanism is related to the protection of mitochondrial membrane, enhanced ability of cells to scavenge oxygen free radicals and reduction of lipid peroxidation.