右美托咪定对H9C2心肌细胞缺氧/复氧损伤的保护作用

Protective Effects of Dexmedetomidine on Hypoxia/Reoxygenation Injury in H9C2 Cardiomyocytes

目的观察右美托咪定对H9C2心肌细胞缺氧/复氧损伤的保护作用。方法 H9C2心肌细胞随机分为三组:正常对照组(Control)、缺氧/复氧组(H/R)、Dex(5μmol/L)干预H/R组。Dex干预H/R组先用Dex预处理6h后,再经缺氧/复氧处理。采用倒置显微镜观察各组H9C2心肌细胞形态的变化,检测各组细胞培养基中LDH的含量,CCK-8法检测各组H9C2心肌细胞的存活率,试剂盒检测caspase-3活性,TUNEL法检测细胞凋亡并计算凋亡指数。结果与Control组相比,H/R组细胞皱缩,大量死亡,细胞活力降低,培养基中LDH含量增加,caspase-3活性增加,细胞凋亡指数增加,统计学意义显著(P<0.01);Dex预处理可明显改善H/R处理后细胞形态,提高细胞活力,减少LDH含量和caspase-3活性,降低细胞凋亡指数,统计学意义显著(P<0.01)。结论 Dex可通过减少H9C2心肌细胞缺氧/复氧引起的细胞凋亡减轻损伤。

Objective To observe the protective effects of dexmedetomidine on hypoxia/reoxygenation injury of H9C2 cardiomyocytes.Methods H9C2 cardiomyocytes were randomly divided into three groups:normal control group(Control),hypoxia/reoxygenation group(H/R)and Dex(5μmol/L)intervention group.Dex intervention in group H/R was treated with Dex pretreatment for 6 h before anoxia/reoxygenation.The morphologic changes of H9C2 cardiomyocytes in each group were observed by inverted microscope.The content of LDH in the cell culture medium of each group was detected.The survival rate of H9C2 cardiomyocytes in each group was detected by CCK-8 method.The activity of caspase-3 was detected by the kit.The apoptosis was detected by TUNEL method and the apoptosis index was calculated.Results Compared with the Control group,the cells in the H/R group were shrinking,a large number of deaths,the decrease of cell vitality,the increase of LDH content in the medium,the increase of the activity of caspase-3,the increase of the apoptosis index,and the significant statistical significance(P<0.01).Dex pretreatment could obviously improve the morphology of the cells after H/R treatment,raise the vitality of the cells,reduce the content of LDH and caspase-3 activity decreased the apoptotic index,and the difference was statistically significant(P<0.01).Conclusion Dex can reduce the injury of H9C2 cardiomyocytes induced by hypoxia/reoxygenation.