期刊
PPAR RESEARCH
卷 2018, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2018/7916953
关键词
-
资金
- Science and Technology Planning Project of Guangdong Province [2016A020226005]
- Natural Science Foundation of Guangdong Province [2015A030310076]
- Nature Scientific Foundation of Guangdong Second Provincial General Hospital [YQ2015-008]
The peroxisome proliferator-activated receptor-a (PPAR-a) agonist fenofibrate ameliorates cardiac hypertrophy; however, its mechanism of action has not been completely determined. Our previous study indicated that a disintegrin and metalloproteinase-17 (ADAM17) is required for angiotensin II-induced cardiac hypertrophy. This study aimed to determine whether ADAM17 is involved in the protective action of fenofibrate against cardiac hypertrophy. Abdominal artery constriction-(AAC-) induced hypertensive rats were used to observe the effects of fenofibrate on cardiac hypertrophy and ADAM17 expression. Primary cardiomyocytes were pretreated with fenofibrate (10 mu M) for 1 hour before being stimulated with angiotensin II (100 nM) for another 24 hours. Fenofibrate reduced the ratios of left ventricular weight to body weight (LVW/BW) and heart weight to body weight (HW/BW), left ventricular anterior wall thickness (LVAW), left ventricular posterior wall thickness (LVPW), and ADAM17 mRNA and protein levels in left ventricle in A AC-induced hypertensive rats. Similarly, in vitro experiments showed that fenofibrate significantly attenuated angiotensin II-induced cardiac hypertrophy and diminished ADAM17 mRNA and protein levels in primary cardiomyocytes stimulated with angiotensin II. In summary, a reduction in ADAM17 expression is associated with the protective action of PPAR-alpha agonists against pressure overload-induced cardiac hypertrophy.
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