摘要
目的探讨瞬时受体电位阳离子通道V亚族成员1(TRPV1)对H9c2心肌细胞缺氧复氧后凋亡的保护作用及可能机制。方法将H9c2心肌细胞随机分为对照组、模型组(缺氧/复氧组)、辣椒素(TRPV1激活剂)组(缺氧/复氧+辣椒素组)、辣椒素+LY组[缺氧/复氧+辣椒素+LY294002(PI3k抑制剂)组]。采用CCK-8法测定心肌细胞存活率,采用流式细胞仪测定各组心肌细胞凋亡率,采用Western blot法和逆转录-聚合酶链反应(RTPCR)法测定各组细胞caspase-3、B淋巴细胞瘤-2基因(Bcl-2)、Bcl-2相关X蛋白(Bax)、磷酸化-蛋白激酶B(pAkt)、蛋白激酶B(Akt)水平。结果与对照组比较,模型组、辣椒素组、辣椒素+LY组心肌细胞存活率和Bcl-2水平降低(均P<0.05),细胞凋亡率和caspase-3、Bax、p-Akt水平升高(均P<0.05);与模型组比较,辣椒素组心肌细胞存活率和Bcl-2、p-Akt水平升高(均P<0.05),细胞凋亡率和caspase-3、Bax水平降低(均P<0.05);模型组与辣椒素+LY组各指标比较差异均无统计学意义(均P>0.05)。结论 TRPV1可抑制缺氧复氧后H9c2心肌细胞凋亡,其机制可能与TRPV1激活磷脂酰肌醇3-激酶(PI3k)/Akt信号通路有关。
Objective To investigate the protective effect and possible mechanism of transient receptor potential cation channel subfamily V member 1(TRPV1) on apoptosis of H9c2 cardiomyocyte after hypoxia-reoxygenation injury.Methods H9c2 cardiomyocyte were randomly divided into control group,model group(hypoxia/reoxygenation),capsaicin group(hypoxia/reoxygenation + capsaicin),capsaicin + LY group(hypoxia/reoxygenation + capsaicin +LY294002).The cell survival rate of cardiomyocyte was determined by CCK-8 method.The apoptosis rate of cardiomyocyte was determined by flow cytometry.Western blot and reverse transcription-polymerase chain reaction(RT-PCR) were used to determine caspase-3,B-cell lymphoma 2 gene(Bcl-2),Bcl-2 related X protein(BAX),phosphoric acid-protein kinase B(p-Akt) and protein kinase B(Akt) levels.Results Compared with the control group,the cell survival rate of cardiomyocyte and the Bcl-2 level in the model group,capsaicin group and capsaicin + LY group decreased(all P < 0.05),the apoptosis rate and the levels of caspase-3,Bax,p-Akt increased(all P < 0.05);Compared with the model group,the cell survival rate of cardiomyocyte and the levels of Bcl-2,p-Akt in the capsaicin group were increased(all P < 0.05),and the apoptosis rate and the levels of caspase-3 and Bax were decreased(all P < 0.05).There were no significant difference in each indexes between the model group and the capsaicin + LY group(all P > 0.05).Conclusion TRPV1 can inhibit H9c2 cardiomyocyte apoptosis after hypoxia-reoxygenation inury,and its mechanism may be related to TRPV1 activation of phosphatidylinositol 3-kinase(PI3k)/Akt signaling pathway.
作者
罗建华
王欢
LUO Jian-hua;WANG Huan(Department of Cardiology,Zhejiang Armed Police Corps Jiaxing Hospital ,Jiaxing ,Zhejiang 314000,China)
出处
《中华全科医学》
2019年第2期200-204,共5页
Chinese Journal of General Practice
基金
浙江省医药卫生科技计划项目(2018KY231)
