Atorvastatin improves left ventricular remodeling and cardiac function in rats with congestive heart failure by inhibiting RhoA/Rho kinase‑mediated endothelial nitric oxide synthase

  • Authors:
    • Liping An
    • Shoukuan An
    • Zhuowen Jia
    • Huan Wang
    • Zhaoying Yang
    • Chaoxin Xu
    • Xiane Teng
    • Jipeng Wang
    • Xiaodong Liu
    • Qidong Cao
    • Sha Wang
  • View Affiliations

  • Published online on: November 16, 2018     https://doi.org/10.3892/etm.2018.6976
  • Pages: 960-966
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Abstract

The aim of the present study was to investigate the effects and possible mechanisms of atorvastatin (Ato) against chronic heart failure (CHF). A rat model of CHF was established and cardiac functions were assessed using Echocardiography. The expression of RhoA/Rho kinase and endothelial nitric oxide synthase (eNOS) was assessed using western blotting and reverse transcription polymerase chain reaction following 4 weeks of treatment. The three groups assessed in the present study were as follows: The control group (no treatment), the Ato + isopropylnoradrenaline (ISO) group (subcutaneous injections of 340 mg/kg ISO + orally administered 50 mg/kg Ato dissolved in saline; administered once daily) and the ISO group (subcutaneous injections of 340 mg/kg ISO + orally administered with an equal volume of saline; administered once daily). Heart volume and weight in the ISO group were significantly increased compared with the control (C) group (P<0.01), whereas contractility was decreased. The results were reverse for the Ato group when compared with the ISO group (P<0.05). Levels of RhoA/Rho kinase protein and mRNA were significantly increased in the ISO group (P<0.01); however. The mRNA and protein expression of eNOS was significantly decreased (P<0.05) when compared with the C group. The mRNA and protein expression of RhoA/Rho kinase was significantly reduced in the Ato+ISO group compared with the ISO group (P<0.01), whereas the mRNA and protein expression of eNOS was significantly increased (P<0.05). RhoA protein expression was increased in the cytoplasm of the C group and on the cell membrane of the ISO group; however, in the Ato+ISO group, RhoA protein expression on the cell membrane was significantly downregulated when compared with the ISO group (P<0.05). The results of the present study suggest that Ato upregulates eNOS by inhibiting RhoA/Rho kinase overexpression in the myocardial tissue of rats with CHF, thus improving left ventricular remodeling and cardiac function.
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January-2019
Volume 17 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
An L, An S, Jia Z, Wang H, Yang Z, Xu C, Teng X, Wang J, Liu X, Cao Q, Cao Q, et al: Atorvastatin improves left ventricular remodeling and cardiac function in rats with congestive heart failure by inhibiting RhoA/Rho kinase‑mediated endothelial nitric oxide synthase. Exp Ther Med 17: 960-966, 2019
APA
An, L., An, S., Jia, Z., Wang, H., Yang, Z., Xu, C. ... Wang, S. (2019). Atorvastatin improves left ventricular remodeling and cardiac function in rats with congestive heart failure by inhibiting RhoA/Rho kinase‑mediated endothelial nitric oxide synthase. Experimental and Therapeutic Medicine, 17, 960-966. https://doi.org/10.3892/etm.2018.6976
MLA
An, L., An, S., Jia, Z., Wang, H., Yang, Z., Xu, C., Teng, X., Wang, J., Liu, X., Cao, Q., Wang, S."Atorvastatin improves left ventricular remodeling and cardiac function in rats with congestive heart failure by inhibiting RhoA/Rho kinase‑mediated endothelial nitric oxide synthase". Experimental and Therapeutic Medicine 17.1 (2019): 960-966.
Chicago
An, L., An, S., Jia, Z., Wang, H., Yang, Z., Xu, C., Teng, X., Wang, J., Liu, X., Cao, Q., Wang, S."Atorvastatin improves left ventricular remodeling and cardiac function in rats with congestive heart failure by inhibiting RhoA/Rho kinase‑mediated endothelial nitric oxide synthase". Experimental and Therapeutic Medicine 17, no. 1 (2019): 960-966. https://doi.org/10.3892/etm.2018.6976