右美托咪定减轻氧化应激改善H9C2细胞缺氧/复氧损伤

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（5 μmol/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。

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

Abstract:Objective To investigate the effect of dexmedetomidine on oxidative stress and improvement of hypoxia/reoxygenation injury in H9C2 cells.Methods H9C2 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 H9C2 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 H9C2 cardiomyocytes by reducing oxidative stress.