天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2014年
7期
641-644
,共4页
郑君毅%王霁翔%肖健勇%丛洪良
鄭君毅%王霽翔%肖健勇%叢洪良
정군의%왕제상%초건용%총홍량
微RNAs%缺氧%肌细胞,心脏%细胞凋亡%miR-1
微RNAs%缺氧%肌細胞,心髒%細胞凋亡%miR-1
미RNAs%결양%기세포,심장%세포조망%miR-1
microRNAs%anoxia%myocytes,cardiac%apoptosis%miR-1
目的:研究微小RNA(miR)-1在缺氧心肌细胞凋亡中的作用。方法将培养的H9C2心肌细胞分为5组,正常对照组、阴性对照组、H2O2组、miR-1组和H2O2+miR-1组。用实时荧光定量PCR方法证实miR-1转染成功后,MTT法和流式细胞术检测细胞存活率和凋亡情况,用PCR和Western Blot的方法检测抗凋亡因子bcl-2的mRNA和蛋白表达情况。结果与正常对照组相比,阴性对照组各个指标的变化差异均无统计学意义。其他3组细胞的miR-1表达水平显著升高,细胞存活率下降,凋亡率增加,Bcl-2的mRNA和蛋白表达水平均明显降低。结论微小RNA-1可通过降低抗凋亡因子Bcl-2的表达水平诱导缺氧心肌细胞的凋亡。
目的:研究微小RNA(miR)-1在缺氧心肌細胞凋亡中的作用。方法將培養的H9C2心肌細胞分為5組,正常對照組、陰性對照組、H2O2組、miR-1組和H2O2+miR-1組。用實時熒光定量PCR方法證實miR-1轉染成功後,MTT法和流式細胞術檢測細胞存活率和凋亡情況,用PCR和Western Blot的方法檢測抗凋亡因子bcl-2的mRNA和蛋白錶達情況。結果與正常對照組相比,陰性對照組各箇指標的變化差異均無統計學意義。其他3組細胞的miR-1錶達水平顯著升高,細胞存活率下降,凋亡率增加,Bcl-2的mRNA和蛋白錶達水平均明顯降低。結論微小RNA-1可通過降低抗凋亡因子Bcl-2的錶達水平誘導缺氧心肌細胞的凋亡。
목적:연구미소RNA(miR)-1재결양심기세포조망중적작용。방법장배양적H9C2심기세포분위5조,정상대조조、음성대조조、H2O2조、miR-1조화H2O2+miR-1조。용실시형광정량PCR방법증실miR-1전염성공후,MTT법화류식세포술검측세포존활솔화조망정황,용PCR화Western Blot적방법검측항조망인자bcl-2적mRNA화단백표체정황。결과여정상대조조상비,음성대조조각개지표적변화차이균무통계학의의。기타3조세포적miR-1표체수평현저승고,세포존활솔하강,조망솔증가,Bcl-2적mRNA화단백표체수평균명현강저。결론미소RNA-1가통과강저항조망인자Bcl-2적표체수평유도결양심기세포적조망。
Objective To investigate the apoptotic effect of microRNA-1 (miR-1) on hypoxemic cardiomyocytes. Methods The cultured H9C2 cells were divided into 5 groups:normal control group, negative control group, H2O2 group, miR-1 group and H2O2+miR-1 group. After verified the success of transfection by real time PCR, MTT and flow cytometry methods were used to test the cell vitality and apoptotic rate, while the mRNA and protein expression level of Bcl-2 were de-tected by real time PCR and Western blot methods. Results Compared with normal control group, there were no significant differences in all indexes in negative control group. The application of H2O2 and miR-1 respectively or together significantly increased the miR-1 level and apoptotic rate, and reduced the cell vitality and Bcl-2 expression level. Conclusion mi-croRNA-1 can induce cardiomyocyte apoptosis by downregulating anti-apoptosis factor Bcl-2.