Reversion of left ventricle remodeling in spontaneously hypertensive rats by valsartan is associated with the inhibition of caspase-3, -8 and -9 activities

Deng,Xu; Xia,Ke; Chen,Po; Ali Sheikh,Md   Sayed; Yang,Da‑Feng; Li,Si‑Min; Yang,Tian‑Lun

doi:10.3892/br.2015.458

Reversion of left ventricle remodeling in spontaneously hypertensive rats by valsartan is associated with the inhibition of caspase-3, -8 and -9 activities

Authors:
- Xu Deng
- Ke Xia
- Po Chen
- Md Sayed Ali Sheikh
- Da‑Feng Yang
- Si‑Min Li
- Tian‑Lun Yang
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Affiliations: Department of Cardiology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China, Hunan Provincial Tumor Hospital, Central South University, Changsha, Hunan 410008, P.R. China, Xiangya Stomatological Hospital, Central South University, Changsha, Hunan 410008, P.R. China
Published online on: April 29, 2015 https://doi.org/10.3892/br.2015.458
Pages: 533-536

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Abstract

The development of hypertension is closely associated with cardiac hypertrophy and apoptosis, and caspase-3, -8 and -9 are key enzymes of apoptosis. The aim of the present study was to evaluate the effects of valsartan on left ventricle hypertrophy and myocardial apoptosis in spontaneously hypertensive rats (SHRs) and to explore the mechanisms for valsartan against apoptosis. A total of 15 SHRs (16 weeks old) were randomly divided into two groups. The SHRs in the valsartan (n=8) and SHR groups (n=7) were fed with valsartan and distilled water for 8 weeks, respectively. Wistar‑Kyoto rats (n=8) were the control group. At the end of the experiments, blood pressure, parameters regarding hypertrophy, apoptosis and activities of caspase‑3, ‑8 and ‑9 were measured. The results showed that valsartan significantly reduced systolic blood pressure and left ventricular hypertrophy, improved left ventricular remodeling, attenuated the myocardial damage and apoptosis, and decreased the activities of caspase‑3, ‑8 and ‑9 in SHRs. In conclusion, valsartan is able to reverse hypertension‑induced left ventricle remodeling, which is associated with, at least in part, its inhibitory effect on myocardial apoptosis in the death receptor‑mediated extrinsic, as well as the mitochondrial‑mediated intrinsic pathways.

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