甲酰基肽受体2介导脂氧素A4减轻缺氧/复氧所致大鼠心肌细胞凋亡的作用

Alleviation effect of formyl peptide receptor 2-mediated lipoxin A4 on hypoxia/reoxygenation-induced apoptosis in rat cardiomyocytes

目的探讨甲酰基肽受体2(FPR2)介导脂氧素A4(LXA4)减轻缺氧/复氧所致大鼠心肌细胞凋亡的作用。方法将大鼠心肌细胞H9C2分为空白对照组、缺氧/复氧组、LXA4处理组。空白对照组细胞不做任何处理,缺氧/复氧组细胞建立缺氧/复氧模型,LXA4处理组细胞在缺氧/复氧处理后给予10 nmol/L LXA4干预。检测各组心肌细胞FPR2 mRNA的表达情况及细胞凋亡情况,并计算凋亡指数。结果缺氧/复氧组、LXA4处理组、空白对照组细胞的FPR2 mRNA相对表达量依次升高,而凋亡指数依次降低(均P<0.05)。结论 LXA4在FPR2介导下减轻了缺氧/复氧损伤导致的心肌细胞凋亡。

Objective To investigate the role of formyl peptide receptor 2(FPR2)-mediated lipoxin A4(LAX4)in alleviating rat cardiomyocyte apoptosis caused by hypoxia/reoxygenation(H/R).Methods The rat cardiomyocytes H9C2 were divided into blank control group,H/R group and LXA4 treatment group.No intervention was conducted in the blank control group,modeling of H/R in the H/R group,and H/R followed by treatment of 10 nmol/L LXA4 in the LXA4 treatment group.The FPR2 mRNA expression and the apoptosis of cardiomyocytes were determined in all groups,and the apoptosis index was calculated.Results The relative expression of FPR2 mRNA of the cells increased and the apoptosis index decreased in the order of the H/R group,the LXA4 treatment group and the blank control group(all P<0.05).Conclusion LXA4 can attenuate the H/R-induced cardiomyocyte apoptosis mediated by FPR2.