卡托普利对左心室肥厚过程中c-myc表达的抑制作用。

Inhibitory effects of captopril on c-myc expression during left ventricular hypertrophy.

作者信息

Su J Z, Chen D G, Wu K G, Chen S C, Hu W Y, Wang X Y, Rui H B, Wang H J, Xu C S

机构信息

Department of Cardiology, First Affiliated Hospital of Fujian Medical University, Fujian Institute of Hypertension, Fuzhou, China.

出版信息

Zhongguo Yao Li Xue Bao. 1998 Nov;19(6):535-40.

PMID:10437140

Abstract

AIM

To study the molecular mechanism of captopril (Cap) on the inhibition of left ventricular hypertrophy (LVH), disclose the expression and distribution of c-myc in different cell types in left ventricle (LV) in spontaneously hypertensive rats (SHR).

METHODS

Cap 100 mg.kg-1.d-1 was given p.o. to SHR. Systolic blood pressure (SBP), left ventricular weight (LVW), and body weight (BW) were measured at 16-wk old. The level of angiotensin II (Ang II), c-myc mRNA, and oncoprotein were determined by immunohistochemical method, Northern blot, and Western blot, respectively.

RESULTS

Cap reduced SBP, LVW/BW in SHR, with a decrease of Ang II and c-myc expression in LV. Local cardial Ang II mainly distributed in cardiomyocytes. Cap inhibited cardial Ang II production and c-myc expression (histochemical staining intensity index, 0.49 +/- 0.04 vs 0.83 +/- 0.24, P < 0.01). The c-myc oncoprotein was prevailingly located in cardiac fibroblasts. The c-myc oncoprotein in Cap treated SHR was lower than that of WKY.

CONCLUSION

High expression of c-myc in fibroblasts played an important role in the development of LVH in SHR. Inhibitory effects of Cap on LVH was associated with a decreased myocardial Ang II and interstitial fibroblasts c-myc expression. The c-myc oncoprotein post-transcriptional translation was also interrupted by Cap.

摘要

目的

研究卡托普利（Cap）抑制左心室肥厚（LVH）的分子机制，揭示c-myc在自发性高血压大鼠（SHR）左心室（LV）不同细胞类型中的表达及分布。

方法

对SHR灌胃给予Cap 100 mg·kg-1·d-1。在16周龄时测量收缩压（SBP）、左心室重量（LVW）和体重（BW）。分别采用免疫组织化学法、Northern印迹法和Western印迹法测定血管紧张素II（Ang II）、c-myc mRNA和癌蛋白水平。

结果

Cap降低了SHR的SBP、LVW/BW，同时LV中Ang II和c-myc表达降低。局部心肌Ang II主要分布于心肌细胞。Cap抑制心肌Ang II生成和c-myc表达（组织化学染色强度指数，0.49±0.04比0.83±0.24，P<0.01）。c-myc癌蛋白主要位于心脏成纤维细胞。Cap处理的SHR中c-myc癌蛋白低于WKY。