柚皮苷抑制低氧/复氧致大鼠心肌细胞系H9c2损伤

目的研究柚皮苷(NAR)对H9c2低氧/复氧(H/R)损伤心肌细胞内质网应激的影响。方法将H9c2心肌细胞随机分为对照组(C组)、低氧/复氧组(H/R组)低氧4 h后复氧24 h、柚皮苷10、20和40μg/mL组。于低氧前6 h给予柚皮苷培养再行低氧4 h后复氧24 h。实验后TUNEL检测心肌细胞凋亡;Western blot检测GRP78、ATF6、Bax及Bcl-2蛋白表达。结果与对照组相比,H/R组细胞凋亡增加,GRP78、ATF6、Bax蛋白表达和Bax/Bcl-2比率显著上调,而Bcl-2蛋白表达显著下调(P<0.05);与H/R组比较,柚皮苷3个剂量组均可使细胞凋亡减少,GRP78、ATF6、Bax、Bax/Bcl-2比率下调,Bcl-2上调(P<0.05),尤其以柚皮苷20和40μg/mL组作用最显著。结论柚皮苷预处理可以降低细胞凋亡,其机制可能与抑制内质网应激有关。

Naringin inhibits hypoxia/ reoxygenation-induced injury of rat cardiomyocyte cell line H9c2

Objective To study the effect of naringin(NAR)on endoplasmic reticulum(ER)stress in cardiomyocytes injured by H9 c2 hypoxia/reoxygenation(H/R).Methods H9 c2 cardiomyocytes were randomly divided into three groups:control group,hypoxia/reoxygenation group(H/R)for 24 h after hypoxia for 4 h,naringin 10,20 and 40μg/mL groups.Naringin was added 6 h before exposed to hypoxia for 4 h and then reoxygenation for 24 h.TUNEL detected apoptosis of cardiomyocytes after the experiment.Western blot was used to detect the expression of GRP78,ATF6,Bax and Bcl-2.Results Compared with control group,the cell apoptosis was increased,the expression of GRP78,ATF6,Bax protein expression and Bax/Bcl-2 were remarkably up-regulated(P<0.05),but Bcl-2 protein expression was remarkably down-regulated in H/R group.Compared with the H/R group,the cell apoptosis decreased;the expression of GRP78,ATF6,Bax and Bax/Bcl-2 were down-regulated(P<0.05),but Bcl-2 was up-regulated in the groups with naringin three groups,especially the 20 and 40μg/mL groups.Conclusions The pretreatment of naringin can reduce the apoptosis of myocardial cell.The mechanism may be related to the inhibition of the apoptotic pathway as a response to endoplasmic reticulum stress.