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目的研究外源重组人生长停滞特异性蛋白6(rhGas6)对缺氧/复氧(H/R)诱导的原代乳鼠心肌细胞及H9c2细胞损伤的影响。方法体外培养新生Wistar大鼠心肌细胞及H9c2细胞,随机各分为3组:正常组、H/R组及rhGas6预处理组(rhGas6组)。观察各组细胞形态及心肌细胞搏动频率,检测细胞存活率、乳酸脱氢酶(LDH)浓度及半胱氨酸蛋白酶(Caspase-3)活性变化,流式细胞仪检测细胞凋亡率。结果原代心肌细胞及H9c2细胞H/R组均较正常组细胞活力下降,凋亡率、LDH及Caspase-3水平均较正常组增高。而Gas6组与H/R组比较,细胞活力增加,凋亡率、LDH及Caspase-3水平均减低(P<0.05)。结论 rhGas6对H/R诱导的原代心肌细胞及H9c2细胞损伤均发挥着潜在的保护作用,并可能是通过抑制Caspase-3活性减少细胞凋亡发挥的。
Objective To investigate the effect of exogenous recombinant human growth arrest specific protein 6 (rhGas6) on the injury of primary neonatal rat cardiomyocytes and H9c2 cells induced by hypoxia / reoxygenation (H / R). Methods The neonatal Wistar rat cardiomyocytes and H9c2 cells were cultured in vitro and randomly divided into 3 groups: normal group, H / R group and rhGas6 pretreatment group (rhGas6 group). Cell morphology and cardiomyocyte pulsation frequency in each group were observed. Cell viability, LDH concentration and caspase-3 activity were measured. Cell apoptosis was detected by flow cytometry. Results The viability of primary cardiomyocytes and H / R cells of H9c2 cells were lower than that of normal cells, and the apoptotic rate, LDH and Caspase-3 levels were significantly higher than those of normal cells. However, compared with H / R group, the cell viability increased, the apoptosis rate, LDH and Caspase-3 levels decreased in Gas6 group (P <0.05). Conclusion rhGas6 plays a potential protective role on H / R-induced primary cardiomyocytes and H9c2 cell injury, and may play a role in reducing apoptosis by inhibiting Caspase-3 activity.