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11 January 2019 : Animal Research  

Atorvastatin Prevents Myocardial Fibrosis in Spontaneous Hypertension via Interleukin-6 (IL-6)/Signal Transducer and Activator of Transcription 3 (STAT3)/Endothelin-1 (ET-1) Pathway

Tianfu Fang1CDE, Baoliang Guo1BCE, Lujing Xue1BCF, Li Wang1AD*

DOI: 10.12659/MSM.912032

Med Sci Monit 2019; 25:318-323

Abstract

BACKGROUND: Hypertension is a leading global disease, and myocardial fibrosis is an important adverse effect of hypertension, seriously threatening human health. The IL-6/STAT3 pathway and endothelin-1 (ET-1) were previously suggested to play a part in myocardial fibrosis.

MATERIAL AND METHODS: To investigate the role of Atorvastatin (Ato) in spontaneous hypertension, systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured, and Masson trichrome staining was performed. Furthermore, the relative protein levels of the IL-6/STAT3/ET-1 pathway were tested.

RESULTS: Ato prevented myocardial fibrosis in spontaneous hypertension rats, especially at the dosage of 50 mg/kg/d. The IL-6/STAT3 pathway was observed to be suppressed by Ato, and ET-1 level in myocardial tissues was also downregulated by Ato. The phosphorylation status of STAT3 was tested after Ato treatment, showing that Ato mainly stimulated the tyr-705 phosphorylation of STAT3.

CONCLUSIONS: Results of this study may help promote myocardial fibrosis therapy and provide insights into the IL-6/STAT3/ET-1-mediated mechanism in Ato-induced myocardial fibrosis inhibition.

Keywords: Endomyocardial Fibrosis, Endothelin-1, Hypertension, Receptors, Interleukin-6, STAT3 Transcription Factor, atorvastatin, Blood Pressure, Cardiomyopathies, Fibrosis, Interleukin-6, Myocardium, Phosphorylation, Rats, Inbred SHR, Rats, Inbred WKY

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750