Secondhand Smoke Exposure Enhances Cardiac Fibrosis Effects on the Aging Rat Hearts.

Autor:	Wu JP; Graduate Institute of Basic Medical Science, China Medical University., Chang-Lee SN; Department of Healthcare Administration, Asia University, Taichung., Day CH; Department of Nursing, MeiHo University, Pingtung., Ho TJ; Graduate Institute of Chinese Medicine, China Medical University, Taichung; ; Chinese Medicine Department, China Medical University Beigang Hospital, Taiwan., Viswanadha VP; Department of Biotechnology, Bharathiar University, Coimbatore, India., Chung LC; Department of Hospital and Health Care Administration, Chia Nan University of Pharmacy & Science, Tainan County., Hwang JM; School of Applied Chemistry, Chung Shan Medical University., Jong GP; Division of Cardiology, Armed Force Taichung General Hospital., Kuo WW; Department of Biological Science and Technology, China Medical University., Huang CY; Graduate Institute of Basic Medical Science, China Medical University; ; Graduate Institute of Chinese Medicine, China Medical University, Taichung; ; Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.
Jazyk:	angličtina
Zdroj:	Acta Cardiologica Sinica [Acta Cardiol Sin] 2016 Sep; Vol. 32 (5), pp. 594-603.
DOI:	10.6515/acs20150824c
Abstrakt:	Background: Examining aging rats exposed to secondhand smoke (SHS) engenders changes in left ventricular remodeling due to age- or disease-dependent alterations. Methods: Rats were placed in whole-body exposure chambers and exposed to 10 cigarettes. Filtered air was introduced into the chamber at a low rate. Rats were exposed to SHS for 30 min, twice a day, 5 days per week for 1 month. After 4 weeks SHS exposure, rats were sacrificed for morphological study with trichome staining and left ventricular remodeling related protein analysis using western blot. Results: Characteristic fibrotic morphology in the left ventricle increased significantly with aging and exposure to SHS. Exposure to SHS elevated TGFβ1/p-Smad2/3/CTGF and MMP2/MMP9 protein expression levels (p < 0.05). No significant differences in FGF-2 and UPA protein expression were noted as a result of SHS exposure. However, TIMP-1, TIMP-2, TIMP-3 and TIMP-4 protein expression were suppressed by SHS exposure. We also observed increased TGFβ1/p-Smad2/3/CTGF (p < 0.01), FGF-2/UPA (p < 0.05) and decreased TIMPs protein expression levels. Corresponding MMP2 and MMP9 upregulation occurred with aging and exposure to SHS. TGFβ1/p-Smad2/3/CTGF and FGF-2/UPA protein expression from SHS exposure were higher than that from aging. In contrast, MMP2 and MMP9 were increased in aging rats compared with SHS exposed rats (p < 0.05); however, TIMP-1 (p < 0.01), TIMP-2 (p < 0.01) and TIMP-3 (p < 0.05) were decreased. TIMP-4 protein expression levels were decreased compared with SHS exposed rats (p < 0.01). Conclusions: Aging and SHS exposure in rats will produce elevated fibrosis. Exposure to SHS will accelerate aging and left ventricular fibrosis.
Databáze:	MEDLINE
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