Zhao H, Gu D W, Li H T, Ge Q F, Li G P
Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China.
Department of Cardiology, Affiliated Hospital of North China University of Science and Technology, Tangshan, China.
Genet Mol Res. 2015 Aug 28;14(3):10315-21. doi: 10.4238/2015.August.28.17.
This study evaluated the inhibitory effects of spironolac-tone, 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, col-lagen 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 ar-eas 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, respec-tively; P < 0.05). However, there were no significant differences in the area of collagen III among the three groups. In conclusion, spi-ronolactone improves myocardial collagen deposition, preventing myocardial fibrosis in SHRs.
本研究评估了非选择性醛固酮受体拮抗剂螺内酯对高血压诱导的心肌纤维化的抑制作用。在给予螺内酯后，检测自发性高血压大鼠（SHRs）心肌组织中I型和III型胶原蛋白的含量。将20只雄性SHRs分为螺内酯组或对照组（每组N = 10）；同时使用7只Wistar-Kyoto大鼠（WKY）。将溶解于双蒸水的螺内酯以20 mg·kg(-1)·day(-1)的剂量经口灌胃给药。同时，对照组和WKY组给予等量的双蒸水，持续16周。采用蛋白质免疫印迹法检测心肌组织中I型胶原蛋白的含量；使用偏光显微镜进行观察，随后计算I型胶原蛋白的面积积分和I/III型胶原蛋白的比例。与WKY组相比，对照组中I型胶原蛋白的合成显著更高（1.87 ± 0.2对1.21 ± 0.7，P < 0.05）。治疗16周后，螺内酯组中I型胶原蛋白的含量显著低于对照组（1.42 ± 0.05对1.87 ± 0.2，P < 0.05）。螺内酯组中I型胶原蛋白的面积和I/III型胶原蛋白的比例显著小于对照组（分别为6400 ± 259对12,019 ± 734像素，15.64 ± 1.34对20.8 ± 3.04像素；P < 0.05）。然而，三组之间III型胶原蛋白的面积没有显著差异。总之，螺内酯可改善心肌胶原沉积，预防SHRs的心肌纤维化。
