@article{APS8995,
author = {Jin-Zi Su and Da-Guang Chen and Ke-Gui Wu and Song-Cang Chen and Wen-Yang Hu and Xiang-Yu Wang and Hong-Bing Rui and Hua-Jun Wang and Chang-Sheng Xu},
title = {Inhibitory effects of captopril on c-myc expression during left ventricular hypertrophy},
journal = {Acta Pharmacologica Sinica},
volume = {19},
number = {6},
year = {2016},
keywords = {},
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.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/8995}
}