Effect of Atorvastatin on Expression of Peroxisome Proliferator-activated Receptor Beta/delta in AngiotensinⅡ-induced Hypertrophic Myocardial CellsIn Vitro

Li Sheng; Xu Yang; Ping Ye; Yong-xue Liu; Chun-guang Han

首页> 外文期刊>中国医学科学杂志（英文版） >Effect of Atorvastatin on Expression of Peroxisome Proliferator-activated Receptor Beta/delta in AngiotensinⅡ-induced Hypertrophic Myocardial CellsIn Vitro

【24h】

Effect of Atorvastatin on Expression of Peroxisome Proliferator-activated Receptor Beta/delta in AngiotensinⅡ-induced Hypertrophic Myocardial CellsIn Vitro

机译：阿托伐他汀对血管紧张素Ⅱ诱导的肥厚性心肌细胞过氧化物酶体增殖物激活受体β/δ表达的影响

获取原文

获取原文并翻译 | 示例

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

页面导航

摘要
著录项
相关主题

摘要

Objective To explore the effect of atorvastatin on cardiac hypertrophy and to determine the potential mechanism involved. Methods Anin vitro cardiomyocyte hypertrophy from neonatal rats was induced with angiotensinⅡ (AngⅡ) stimulation. Before AngⅡ stimulation, the cultured rat cardiac myocytes were pretreated with atorvastatin at different concentrations (0.1, 1, and 10μmol/L). The following parameters were evaluated: the myocyte surface area,3H-leucine incorporation into myocytes, mRNA expressions of atrial natriuretic peptide, brain natriuretic peptide, matrix metalloproteinase 9, matrix metalloproteinase 2, and interleukin-1β, mRNA and protein expressions of theδ/β peroxisome proliferator-activated receptor (PPAR) subtypes. Results It was shown that atorvastatin could ameliorate AngⅡ-induced neonatal cardiomyocyte hypertrophy in the area of cardiomyocytes,3H-leucine incorporation, and the expression of atrial natriuretic peptide and brain natriuretic peptide markedly. Meanwhile, atorvastatin also inhibited the augmented mRNA level of several cytokines in hypertrophic myocytes. Furthermore, the down-regulated expression of PPAR-δ/β at both the mRNA and protein levels in hypertrophic myocytes could be significantly reversed by atorvastatin treatment. Conclusions Atorvastatin could improve AngⅡ-induced cardiac hypertrophy and inhibit the expression of cytokines. Such effect might be partly achieved through activation of the PPAR-δ/β pathway.

机译：目的探讨阿托伐他汀对心脏肥大的影响，并探讨其潜在机制。方法采用血管紧张素Ⅱ（AngⅡ）刺激新生大鼠体外心肌肥大。在AngⅡ刺激之前，用不同浓度（0.1、1和10μmol/ L）的阿托伐他汀预处理培养的大鼠心肌细胞。评价以下参数：心肌细胞表面积，3 H-亮氨酸掺入心肌细胞，心房利钠肽，脑利钠肽，基质金属蛋白酶9，基质金属蛋白酶2和白介素-1β的mRNA表达，δ/β的mRNA和蛋白质表达过氧化物酶体增殖物激活受体（PPAR）亚型。结果表明，阿托伐他汀能改善AngⅡ诱导的心肌细胞肥大，3H-亮氨酸掺入，心钠素和脑钠素的表达。同时，阿托伐他汀还抑制肥厚性肌细胞中几种细胞因子的mRNA水平升高。此外，阿托伐他汀治疗可以显着逆转肥厚性心肌细胞中PPAR-δ/βmRNA和蛋白水平的下调。结论阿托伐他汀可以改善AngⅡ引起的心肌肥大并抑制细胞因子的表达。可以通过激活PPAR-δ/β途径部分实现这种效果。

著录项

来源
《中国医学科学杂志（英文版）》 |2015年第4期|245-251|共7页
作者
Li Sheng; Xu Yang; Ping Ye; Yong-xue Liu; Chun-guang Han;
展开▼
作者单位

Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853, China;

Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853, China;

Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853, China;

Department of Pharmacology & Toxicology, Beijing Institute of Radiation Medicine, Beijing 100850, China;

Department of Pharmacology & Toxicology, Beijing Institute of Radiation Medicine, Beijing 100850, China;

展开▼
收录信息中国科学引文数据库(CSCD);中国科技论文与引文数据库(CSTPCD);
原文格式 PDF
正文语种 eng
中图分类
关键词

Effect of Atorvastatin on Expression of Peroxisome Proliferator-activated Receptor Beta/delta in AngiotensinⅡ-induced Hypertrophic Myocardial CellsIn Vitro

摘要

著录项

相关主题

期刊订阅