TAX1结合蛋白1加重苯肾上腺素诱导的心肌细胞凋亡  

TAX1BP1 aggravates phenylephrine-induced apoptosis of cardiomyocytes

作　　者：谢青文 吴青青[1] 唐其柱[1] Xie Qingwen;Wu Qingqing;Tang Qizhu(Department of Cardiology,Renmin Hospital of Wuhan University,Hubei Key Laboratory of Metabolic and Chronic Diseases,Wuhan 430060,Hubei Province,China)

机构地区：[1]武汉大学人民医院心血管内科代谢与相关慢病湖北省重点实验室,430060

出　　处：《中华老年心脑血管病杂志》2022年第1期74-77,共4页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

基　　金：国家自然科学基金(81530012);国家重点研发计划(2018YFC1311300)。

摘　　要：目的探究TAX1结合蛋白1(TAX1BP1)对苯肾上腺素(PE)诱导的原代新生大鼠心肌细胞(NRCM)凋亡的影响。方法将培养的NRCM分为正常组、模型组(PE 50μmol/L)、阴性组、转染组(转染TAX1BP1过表达腺病毒)、对照组、刺激组(转染TAX1BP1过表达腺病毒后,用PE 50μmol/L)。采用α肌动蛋白免疫荧光染色观察NRCM面积,TUNEL染色检测NRCM凋亡程度,免疫印迹法检测TAX1BP1及促凋亡因子Bax和抗凋亡因子Bcl-2蛋白表达。结果模型组NRCM中TAX1BP1表达较正常组明显升高(0.97±0.16 vs 0.69±0.06,P<0.05)。与阴性组相比,转染组NRCM中的TAX1BP1表达上调(0.98±0.08 vs 0.65±0.07,P<0.05);与转染组相比,刺激组NRCM中的TAX1BP1表达上调(1.24±0.06 vs 0.98±0.08,P<0.05)。与阴性组比较,对照组NRCM面积增大、NRCM凋亡数量增加、Bax蛋白表达增加,Bcl-2蛋白表达减少(P<0.05);与对照组比较,刺激组NRCM面积增大、NRCM凋亡数量增加,Bax蛋白表达上调,Bcl-2蛋白表达下调(P<0.05)。结论TAX1BP1可促进PE诱导的心肌细胞肥大,通过增加Bax表达以及抑制Bcl-2来加重PE诱导的心肌细胞凋亡。Objective To study the effect of TAX1BP1 on phenylephrine-induced apoptosis of NRCM.Methods The cultured NRCM were divided into normal group,model group(50μmol/L PE),negative group,transfection group(transfecting Ad-TAX1BP1),control group,stimulation group(transfecting Ad-TAX1BP1+50μmol/L PE).The area of NRCM was measured withα-ac-tin immunofluorescence staining.The apoptosis of NRCM was assayed with TUNEL staining.The expressions of TAX1BP1,Bax and Bcl-2 proteins were detected by Western bot.Results The expression level of TAX1BP1 protein was significantly higher in model group than in normal group(0.97±0.16 vs 0.69±0.06,P<0.05),in transfection group than in negative group(0.98±0.08 vs 0.65±0.07,P<0.05),and in stimulation group than in transfection group(1.24±0.06 vs 0.98±0.08,P<0.05).The area of NRCM was significantly larger,the number of apoptosed NRCM was significantly greater,the expression level of Bax was significantly higher while that of Bcl-2 was significantly lower in control group than in negative group and in stimulation group than in control group(P<0.05).Conclusion TAX1BP1 promotes PE-induced hypertrophy and apoptosis of NRCM by upregulating the expression of Bax and inhibiting that of Bcl-2.

关 键 词：肌细胞 心脏 细胞凋亡 心力衰竭 转染 苯福林 

分 类 号：R541.6[医药卫生—心血管疾病]