右美托咪定减轻氧化应激改善H9C2细胞缺氧/复氧损伤

Dexmedetomidine Alleviated Oxidative Stress and Improved Hypoxia/Reoxygenation Injury in H9C2 Cells

目的探讨右美托咪定减轻氧化应激改善H9C2细胞缺氧/复氧损伤的作用。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6 h后,再经缺氧/复氧处理。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,试剂盒检测MDA的含量和SOD活性。结果与Control组相比,H/R组细胞活力降低,培养基中LDH含量增加,caspase-3活性增加,MDA含量升高而SOD活性降低,统计学意义显著(P<0.01);Dex预处理提高H/R处理后的细胞活力,减少LDH含量和caspase-3活性,降低MDA含量,增加SOD活性,统计学意义显著(P<0.01)。结论Dex可通过减轻氧化应激改善H9C2心肌细胞缺氧/复氧损伤。

Objective To investigate the effect of dexmedetomidine on oxidative stress and improvement of hypoxia/reoxygenation injury in H9 C2 cells.Methods H9 C2 cardiomyocytes were randomly divided into three groups.The normal control group（Control）,hypoxia/reoxygenation group（H/R）,and Dex（5μmol/L）were used to intervene in the H/R group.Dex intervention in the H/R group was pretreated with Dex for 6 h and then treated with hypoxia/reoxygenation.The LDH content in the cell culture medium was detected.The survival rate of H9 C2 cardiomyocytes in each group was detected by CCK-8 method.The caspase-3 activity was detected in the kit, and the MDA content and SOD activity were detected by the kit.Results Compared with the Control group,the cell viability in the H/R group decreased,the LDH content in the medium increased,the caspase-3 activity increased,the MDA content increased and the SOD activity decreased,statistically significant（P〈0.01）;Dex pretreatment improved cell viability after H/R treatment,decreased LDH content and caspase-3 activity,decreased MDA content,and increased SOD activity,with statistical significance（ P 〈0.01）.Conclusion Dex can alleviate hypoxia/reoxygenation injury of H9 C2 cardiomyocytes by reducing oxidative stress.