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Effects of short-chain acyl-CoA dehydrogenase on collagen expression and proliferation of rat cardiac fibroblasts
Authors:SHU Zhao-hui  ZENG Zhen-hua  HUANG Qiu-ju  LI Zhong-hong  LIU Pei-qing  CHEN Shao-rui  LAN Tian  ZANG Lin-quan  ZHOU Si-gui
Institution:1. Department of Clinical Pharmacy, Guangdong Pharmaceutical University, Guangzhou 510006, China; 2. Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China
Abstract:AIM: To investigate the effect of short-chain acyl-CoA dehydrogenase (SCAD) on collagen expression and proliferation of rat cardiac fibroblasts and to explore the relationship between SCAD and cardiac fibrosis. METHODS: The model of proliferation and collagen expression of rat cardiac fibroblasts induced by angiotensin II was established. After treatment with siRNA-1186, the expression of SCAD at mRNA and protein levels, fatty acids beta oxidation rate, ATP, the enzyme activity of SCAD and free fatty acids in the rat cardiac fibroblasts were determined. RESULTS: The mRNA and protein expression of SCAD was decreased in the rat cardiac fibroblasts induced by angiotensin II compared with the control cells, and the expression of collagen I and collagen III was significantly upregulated. Compared with negative control group, SCAD expression and activity, fatty acid beta-oxidation rate and ATP significantly decreased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the rat cardiac fibroblasts, and the expression of collagen I and collagen III was significantly up-regulated. CONCLUSION: The expression and synthesis disorder of collagen may be triggered by down-regulation of SCAD. SCAD may be a promising therapeutic target for myocardial fibrosis.
Keywords:Short-chain acyl-CoA dehydrogenase  Cardiac fibroblasts  Myocardial fibrosis  Energy metabolism  Collagen  
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