Ghrelin对AngⅡ诱导的心肌细胞凋亡的影响及机制  

Effect and Mechanism of Ghrelin on H9c2 Cardiomyocytes apoptosis induced by AngⅡ

作　　者：杨春艳[1] 冯朝晖[1] 杨萍[1] 任平[2] 

机构地区：[1]吉林大学中日联谊医院心内科,吉林长春130033 [2]吉林大学第一医院胸外科

出　　处：《中国实验诊断学》2017年第11期1982-1987,共6页Chinese Journal of Laboratory Diagnosis

基　　金：国家自然科学基金(81570360;81400298)

摘　　要：目的阐明Ghrelin对血管紧张素Ⅱ(AngⅡ)诱导的心肌细胞凋亡的影响及其可能机制。方法体外培养H9C2心肌细胞,分为空白对照组、AngⅡ组、AngⅡ+Ghrelin组及单纯Ghrelin组,采用MTT法检测细胞存活率,TUNEL染色观察心肌细胞凋亡情况,并应用RT-PCR法检测Bcl-2、Bax、Caspase-3、1型及2型AngⅡ受体(AT1R,AT2R)mRNA表达。结果与空白对照组相比,AngⅡ组心肌细胞存活率明显下降;细胞凋亡数目明显增加;Caspase-3及促凋亡分子Bax表达明显增加,而抗凋亡分子Bcl-2表达明显减少;AT1R及AT2R表达均明显增加,AT1R增加尤为显著。与AngⅡ组相比,Ghrelin+AngⅡ组心肌细胞存活率明显增加;细胞凋亡数目明显减少;Caspase-3及促凋亡分子Bax表达明显减少,而抗凋亡分子Bcl-2表达明显增加;AT1R表达明显减少,而AT2R表达无明显变化。结论 AT1R及AT2R均参与AngⅡ诱导心肌细胞凋亡进程,Ghrelin可抑制AngⅡ诱导的心肌细胞凋亡,其机制可能与Ghrelin下调通过下调AT1R表达有关。Objective To clarify the effect and possible mechanism of ghrelin on H9c2 cardiomyocytes apoptosis induced by Angiotensin Ⅱ （Ang Ⅱ ）. Methods H9c2 cells were cultured and divided into blank control group,group of Ang H and Ang Ⅱ ＋ Ghrelin and Ghrelin group. MTT was used to detect cell survival,TUNEL staining was used to observe the apoptosis of H9c2 cells,and the RT-PCR was used to detect the mRNA expression of bcl-2,Bax,Caspase- 3,type 1 and type 2 Ang Ill receptors （AT1R,AT2R）. Results Compared with the control group, the survival rate of H9c2 cells decreased significantly in Ang Ⅱ group. The number of apoptosis was significantly increased. The expression of Caspase-3 and Bax was significantly increased,while the expression of bcl-2 was significantly decreased. AT1R and AT2R were significantly increased,especially AT1R. However, ghrelin could significantly increase the survival rate of myocardial cells, reduce the number of apoptosis, down-regulate the expression of Caspase 3, Bax and AT1R, and upregulate the expression of bcl-2. Interestingly,there was no significant change in AT2R expression. Conclusion AT1R and AT2R were both involved in the induction of myocardial apoptosis in Ang Ⅱ. Ghrelin inhibited the apoptosis of my ocardial cells induced by Ang Ⅱ ,and its mechanism could be related to the down-regulation of AT1R.

关 键 词：GHRELIN 血管紧张素Ⅱ 心肌细胞凋亡 血管紧张素Ⅱ受体 

分 类 号：R54[医药卫生—心血管疾病]