返回 
加入收藏
槲皮素通过ACE2-Ang-（1-7）-Mas轴对AngⅡ诱导下大鼠心肌收缩蛋白表达的影响
x
请在关注微信后，向客服人员索取文件
| 篇名： | 槲皮素通过ACE2-Ang-（1-7）-Mas轴对AngⅡ诱导下大鼠心肌收缩蛋白表达的影响 |
| TITLE： | Effects of Quercetin on the Expression of Ang Ⅱ-induced Myocardial Contractile Protein of Rats through ACE 2- Ang-（1-7）-Mas Axis |
| 摘要： | 目的：探讨槲皮素（Que）通过血管紧张素转换酶2-血管紧张素-（1-7）-Mas轴[ACE2-Ang-（1-7）-Mas轴]对血管紧张素Ⅱ（AngⅡ）诱导下原代大鼠心肌收缩蛋白表达的影响。方法：取1～2d日龄大鼠的心肌组织，分离、培养原代心肌细胞，并构建心肌细胞ACE2基因沉默模型。实验分为12组，其中AngⅡ组、AngⅡ+小干扰RNA（siRNA）组、AngⅡ+A779组为模型组，AngⅡ+氯沙坦组为阳性对照组，AngⅡ+Que40组、AngⅡ+Que80组、AngⅡ+siRNA+Que40组、AngⅡ+siRNA+Que80组、AngⅡ+A779+Que40组、AngⅡ+A779+Que80组为实验组，另设空白组、siRNA组。其中AngⅡ终浓度为1×10－6mol/L，siRNA终浓度为50nmol/L，Que终浓度分别为40、80μmol/L，A779（Mas受体拮抗剂）终浓度为1μmol/L，氯沙坦终浓度为1×10－4mol/L。分别检测各组心肌细胞中ACE2、Ang-（1-7）、Mas的mRNA和蛋白表达水平，以及Na+/Ca2+交换通道（NCX）、钙泵（SERCA2a）、磷蛋白（PLB）等3种心肌收缩蛋白的表达水平。结果：与AngⅡ组比较，AngⅡ+Que80组细胞中的MasmRNA表达水平升高（P＜0.05）；AngⅡ+氯沙坦组细胞中的ACE2、MasmRNA表达水平升高（P＜0.05）。与AngⅡ组比较，AngⅡ+Que40组细胞中的ACE2、Ang-（1-7）蛋白表达水平升高（P＜0.05）；与AngⅡ+siRNA组比较，仅AngⅡ+siRNA+Que40组Ang-（1-7）蛋白表达水平升高（P＜0.05）；与AngⅡ+A779组比较，仅AngⅡ+A779+Que40组Ang-（1-7）蛋白表达水平升高（P＜0.05）。与AngⅡ组比较，AngⅡ+Que40组NCX蛋白表达水平降低（P＜0.05），AngⅡ+氯沙坦组NCX蛋白表达水平降低（P＜0.05）；与AngⅡ+A779组比较，AngⅡ+A779+Que80组NCX蛋白表达水平降低（P＜0.05）。结论：Que一定程度上提高了AngⅡ诱导大鼠心肌细胞模型中ACE2-Ang-（1-7）-Mas轴的表达，从而调节心肌收缩蛋白。 |
| ABSTRACT： | OBJECTIVE：To in vestigate the effects of quercetin （Que）on the expressio n of angiotensin Ⅱ（AngⅡ）-induced myocardial contractile proteins of primary rats through angiotensin-converting enzyme 2-angiotensin-（1-7）-Mas （ACE2-Ang- （1-7）-Mas）axis. METHODS ：Cardiac tissue of rats aged 1-2 d were collected ，and primary cardiomyocytes were isolated and cultured. The gene silencing model of cardiomyocytes ACE2 was constructed. Experiments were divided into 12 groups. Among them，AngⅡ group，AngⅡ+ small interference RNA （siRNA）group，and Ang Ⅱ+ A 779 group were the model groups ；AngⅡ+ losartan group was positive control group ；AngⅡ+Que40 group，AngⅡ+Que80 group，AngⅡ+siRNA+Que40 group，AngⅡ+ siRNA+Que80 group，AngⅡ+A779+Que40 group and Ang Ⅱ+A779+Que80 group were the experimental groups ；blank group and siRNA group were set up. Ang Ⅱ concentration was 1×10－6 mol/L；siRNA final concentration was 50 nmol/L；Que concentration was 40 and 80 μmol/L；A779（Mas receptor inhibitor ）concentration was 1 μmol/L；losartan concentration was 1×10－4 mol/L. mRNA and protein expression of ACE 2，Ang-（1-7） and Mas in primary cardiomyocytes were detected ；the expressions of myocardial contractile proteins were also determined ，such as Na +/Ca2+ exchange channel （NCX），calcium pump （SERCA2a）， phosphoprotein （PLB）. RESULTS ：Compared with Ang Ⅱ group，mRNA expression of Mas was increased significantly in Ang Ⅱ + Que 80 group （P＜0.05）；mRNA expression of ACE2 and Mas were increased significantly in Ang Ⅱ + CZ0210-01） losartan group （P＜0.05）. Compared with Ang Ⅱ group，the 851136165@qq.com protein expression of ACE 2 and Ang- （1-7） were increased significantly in Ang Ⅱ+ Que 40 group（P＜0.05）；compared with Ang Ⅱ + siRNA group ，the protein expression of Ang-（1-7）were increased significantly in Ang Ⅱ+ siRNA+Que 40 group（P＜0.05）；compared with Ang Ⅱ+A779 group，the protein expression of Ang- （1-7）were increased significantly in Ang Ⅱ+A779+ Que 40 group（P＜0.05）. Compared with Ang Ⅱ group，the protein expression of NCX was decreased in Ang Ⅱ+Que40 group（P＜0.05），protein expression of NCX was reduced in Ang Ⅱ+ losartan group （P＜0.05）；compared with Ang Ⅱ+A779 group，the protein expression of NCX was decreased in Ang Ⅱ+A779+ Que80 group （P＜0.05）. CONCLUSIONS ：Que improves the expression of Ang Ⅱ -induced ACE 2-Ang-（1-7）-Mas axis in cardiomyocyte model to some extent ，so as to regulate myocardial contractile protein. |
| 期刊： | 2021年第32卷第23期 |
| 作者： | 贾梦楠，朱明军，王永霞，李彬，郝轩轩，王新陆，于瑞，常鑫迪，李洁薇 |
| AUTHORS： | JIA Mengnan， ZHU Mingjun，WANG Yongxia，LI Bin，HAO Xuanxuan，WANG Xinlu，YU Rui，CHANG Xindi，LI Jiewei |
| 关键字： | 槲皮素；血管紧张素转换酶2-血管紧张素（1-7）-Mas轴；心肌细胞；血管紧张素Ⅱ；心肌收缩蛋白 |
| KEYWORDS： | Quercetin；ACE2-Ang-（1-7）-Mas axis ；Cardiomyocytes；Angiotensin Ⅱ；Myocardial contractile protein |
| 阅读数： | 195 次 |
| 本月下载数： | 6 次 |
* 注：未经本站明确许可，任何网站不得非法盗链资源下载连接及抄袭本站原创内容资源!在此感谢您的支持与合作！
