| 引用本文: |
孙涛,李雅,郭志华,龙云,曾英,王月.益心泰对慢性心力衰竭大鼠心室重构及p-p38MAPK、β-arrestin蛋白表达的影响[J].湖南中医药大学学报,2020,40(9):1090-1093[点击复制] |
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| 益心泰对慢性心力衰竭大鼠心室重构及p-p38MAPK、β-arrestin蛋白表达的影响 |
| 孙涛,李雅,郭志华,龙云,曾英,王月 |
| (湖南中医药大学第一附属医院, 湖南 长沙 410007;湖南中医药大学, 湖南 长沙 410208) |
| 摘要: |
| 目的 探讨β-抑制蛋白（β-arrestin）、磷酸化p38丝裂原活化蛋白激酶（p-p38MAPK）蛋白表达对慢性心力衰竭大鼠心室重构的影响及益心泰丸对其干预作用。方法 制备慢性心力衰竭大鼠模型。随机分成正常对照组、模型组、益心泰组和卡维地洛组。益心泰组2.0 g/（10 mL·kg）；卡维地洛组10 mg/（10 mL·kg）；正常对照组及模型组生理盐水等容积灌胃，用药8周后分别检测心室重量指数、左心室内径及β-arrestin、p-p38MAPK蛋白表达情况。结果 与正常对照组比较，模型组左、右心室重量指数明显增加，左室舒张末期内径、收缩末期内径明显增大，左室后壁、室间隔厚度明显降低，β-arrestin蛋白表达下降，p-p38MAPK蛋白表达增加，差异有统计学意义（P<0.01）。与模型组比较，益心泰组和卡维地洛组左、右心室重量指数均降低，左室舒张末期内径、收缩末期内径缩小，左室后壁、室间隔厚度增加，β-arrestin蛋白表达增加，p-p38MAPK蛋白表达下降，差异有统计学意义（P<0.05）；益心泰组与卡维地洛组各项指标组间比较，差异无统计学意义（P>0.05）。结论 益心泰可能通过激活β-arrestin，进而抑制p-p38MAPK蛋白表达，从而在一定程度上干预了心室重构的进程。 |
| 关键词: 慢性心力衰竭 益心泰 心室重构 β-抑制蛋白 p38丝裂原活化蛋白激酶 |
| DOI：10.3969/j.issn.1674-070X.2020.09.009 |
| 投稿时间：2019-11-05 |
| 基金项目:国家自然科学基金项目（81673955）；湖南省中医药科研计划项目（201833）。 |
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| Effects of Yixintai on Ventricular Remodeling and p-p38MAPK, β-arrestin Protein Expression in Rats with Chronic Heart Failure |
| SUN Tao,LI Ya,GUO Zhihua,LONG Yun,ZENG Ying,WANG Yue |
| (The First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China;Hunan University of Chinese Medicine, Changsha, Hunan 410208, China) |
| Abstract: |
| Objective To investigate the effects of β-arrestin and p38 mitogen activated protein kinase (p-p38MAPK) on ventricular remodeling in rats with chronic heart failure and the intervention of Yixintai. Methods The rat model of chronic heart failure was established. The rats were randomly divided into a normal control group, a model group, a Yixintai group and a carvedilol group. The Yixintai group was given drug of 2.0 g/(10 mL·kg); the carvedilol group was given drug of 10 mg/(10 mL·kg); the normal control group and the model group were given normal saline by gavage with equal volume. Ventricular weights index, left ventricular diameter and β-arrestin, p-p38MAPK protein expression were measured after 8 weeks of treatment. Results Compared with the normal control group, the left and right ventricular mass indexes of the model group increased significantly, and the end-diastolic and end-systolic diameters of the left ventricle increased significantly. The thickness of the posterior wall of the left ventricle and the ventricular septum decreased significantly, and the expression of β-arrestin protein decreased. The expression of p-p38MAPK protein increased, and the difference was statistically significant (P<0.01). Compared with the model group, the left and right ventricular mass indexes of the Yixintai group and the carvedilol group were reduced, and the left ventricular end-diastolic and end-systolic diameters decreased. The thickness of the left ventricular posterior wall and ventricular septum increased, and β-arrestin protein expression increased. The expression of p-p38MAPK protein decreased, and the difference was statistically significant (P<0.05). There was no significant difference between the Yixintai group and the carvedilol group in each index, and the difference was statistically significant (P>0.05). Conclusion Yixintai may inhibit the expression of p-p38MAPK by activating β-arrestin, which may interfere with the process of ventricular remodeling to some extent. |
| Key words: chronic heart failure Yixintai ventricular remodeling β-inhibitory protein p38 mitogen activated protein kinase |
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