Research Article

Inhibitory effects of spironolactone on myocardial fibrosis in spontaneously hypertensive rats

Published: August 28, 2015
Genet. Mol. Res. 14 (3) : 10315-10321 DOI: https://doi.org/10.4238/2015.August.28.17
Cite this Article:
(2015). Inhibitory effects of spironolactone on myocardial fibrosis in spontaneously hypertensive rats. Genet. Mol. Res. 14(3): gmr6065. https://doi.org/10.4238/2015.August.28.17
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Abstract

This study evaluated the inhibitory effects of spironolac­tone, a non-selective aldosterone receptor antagonist, on hypertension-induced myocardial fibrosis. Collagen I and III contents was detected in the myocardial tissue of spontaneously hypertensive rats (SHRs) after spironolactone administration. Twenty male SHRs were assigned to the spironolactone group or control group (N = 10 each); 7 Wistar-Kyoto rats (WKY) were also used. Spironolactone dissolved in ddH2O was administered via gavage at a dosage of 20 mg·kg-1·day-1. Meanwhile, the control and WKY groups were administered equivalent volumes of ddH2O for 16 weeks. Western blotting was used to detect the contents of collagen I in myocardial tissue; observations were performed using polarizing microscopy, and the area integration and ratio of collagen I/III were subsequently calculated. Compared to the WKY group, col­lagen I synthesis was significantly higher in the control group (1.87 ± 0.2 vs 1.21 ± 0.7, P < 0.05). After 16 weeks of treatment, collagen I contents were significantly lower in the spironolactone group than in the control group (1.42 ± 0.05 vs 1.87 ± 0.2, P < 0.05). The ar­eas of collagen I and collagen I/III ratio were significantly smaller in the spironolactone group than in the control group (6400 ± 259 vs 12,019 ± 734 pixels, 15.64 ± 1.34 vs 20.8 ± 3.04 pixels, respec­tively; P < 0.05). However, there were no significant differences in the area of collagen III among the three groups. In conclusion, spi­ronolactone improves myocardial collagen deposition, preventing myocardial fibrosis in SHRs

This study evaluated the inhibitory effects of spironolac­tone, a non-selective aldosterone receptor antagonist, on hypertension-induced myocardial fibrosis. Collagen I and III contents was detected in the myocardial tissue of spontaneously hypertensive rats (SHRs) after spironolactone administration. Twenty male SHRs were assigned to the spironolactone group or control group (N = 10 each); 7 Wistar-Kyoto rats (WKY) were also used. Spironolactone dissolved in ddH2O was administered via gavage at a dosage of 20 mg·kg-1·day-1. Meanwhile, the control and WKY groups were administered equivalent volumes of ddH2O for 16 weeks. Western blotting was used to detect the contents of collagen I in myocardial tissue; observations were performed using polarizing microscopy, and the area integration and ratio of collagen I/III were subsequently calculated. Compared to the WKY group, col­lagen I synthesis was significantly higher in the control group (1.87 ± 0.2 vs 1.21 ± 0.7, P < 0.05). After 16 weeks of treatment, collagen I contents were significantly lower in the spironolactone group than in the control group (1.42 ± 0.05 vs 1.87 ± 0.2, P < 0.05). The ar­eas of collagen I and collagen I/III ratio were significantly smaller in the spironolactone group than in the control group (6400 ± 259 vs 12,019 ± 734 pixels, 15.64 ± 1.34 vs 20.8 ± 3.04 pixels, respec­tively; P < 0.05). However, there were no significant differences in the area of collagen III among the three groups. In conclusion, spi­ronolactone improves myocardial collagen deposition, preventing myocardial fibrosis in SHRs

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