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白藜芦醇通过ERK1/2-CREB信号通路抑制血管紧张素Ⅱ诱导的心肌肥大

发表时间:2013-12-15  浏览量:1098  下载量:317
全部作者: 黄勇攀,石刚刚
作者单位: 贵阳医学院药理学教研室;汕头大学医学院
摘 要: 目的:研究白藜芦醇(resveratrol, Resv)对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导H9C2细胞肥大的抑制作用及对细胞外调节蛋白激酶1/2(extracellular regulated protein kinases1/2, ERK1/2)cAMP反应元件结合蛋白(cAMP-response element binding protein,CREB)信号通路的影响。方法:通过建立AngⅡ诱导H9C2细胞肥大模型,采用Image Pro Plus 6.1软件测量细胞表面积大小;二辛可酸(bicinchonini acid,BCA)法测定细胞总蛋白含量,Western blotting检测H9C2细胞株ERK1/2、磷酸化细胞外调节蛋白激酶(phosphated extracellular regulated protein kinases1/2,p-ERK1/2)、CREB和磷酸化cAMP反应元件结合蛋白(phosphated cAMP-response element binding protein,p-CREB)的表达。结果:与对照组相比,添加AngⅡ(0.1 μmol/L)孵育后,细胞表面积增加,细胞蛋白含量增加了46%(P<0.01). Resv(0.01 μmol/L+AngⅡ,0.1 μmol/L+Ang Ⅱ,1 μmol/L+AngⅡ)能浓度依赖地减少蛋白含量。AngⅡ诱导H9C2细胞p-ERK1/2和p-CREB蛋白表达的升高。不同剂量Resv对AngⅡ诱导H9C2细胞p-ERK1/2和p-CREB蛋白的表达均有抑制作用,并且呈浓度依赖。结论:Resv抑制AngⅡ介导的H9C2细胞肥厚,其机制可能是通过抑制细胞表面积增大、细胞蛋白含量增多和干扰ERK1/2-CREB信号通路实现。
关 键 词: 药理学;白藜芦醇;血管紧张素Ⅱ;心肌肥大
Title: Resveratrol inhibits angiotensinⅡ-induced cardiac hypertrophy via the ERK1/2-CREB signaling pathway
Author: HUANG Yongpan, SHI Ganggang
Organization: Department of Pharmacology, Guiyang Medical University; Medical College, Shantou University
Abstract: Objective: To investigate the inhibitory effects of resveratrol (Resv) on angiotensinⅡ (AngⅡ) induced cardiac hypertrophy in H9C2 cell and elucidate the extracellular regulated protein kinases 1/2 (ERK1/2)-cAMP-response element binding protein (CREB) signaling pathway mechanism of cardiac hypertrophy. Methods: AngⅡ was administered to establish the cardiacmyocytes hypertrophy model of H9C2 cells. The cell surface area of H9C2 cells was measured by Image Pro Plus 6.1 software. The total protein content of H9C2 cells was detected by bicinchonini acid (BCA) method. The protein expressionof ERK1/2, phosphated extracellular regulated protein kinases1/2 (p-ERK1/2), CREB and phosphated cAMP-response element binding protein (p-CREB) were detected by Western blotting. Results: Compared with the control group, cell surface area was increased significantly and the total protein content increased 46% (P<0.01) in AngⅡ group. Resv (0.01 μmol/L+AngⅡ, 0.1 μmol/L+AngⅡ, 1 μmol/L+AngⅡ) groups of total protein content decreased in a concentration-dependent manner. AngⅡ stimulated the expression of ERK1/2 and CREB protein. Resv could inhibit the of p-ERK1/2and p-CREB protein induced by AngⅡ in H9C2 cells in a concentration-dependent manner. Conclusion: Resv inhibited AngⅡ-mediated cardiac hypertrophy, the mechanism may be through inhibiting the cell surface area increase, the cell protein content increase and interferring the ERK1/2-CREB signaling pathway.
Key words: pharmacology; resveratrol; angiotensin Ⅱ; cardiac hypertrophy
发表期数: 2013年12月第23期
引用格式: 黄勇攀,石刚刚. 白藜芦醇通过ERK1/2-CREB信号通路抑制血管紧张素Ⅱ诱导的心肌肥大[J]. 中国科技论文在线精品论文,2013,6(23):2230-2234.
 
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