篇名 | Secondhand Smoke Exposure Enhances Cardiac Fibrosis Effects on the Aging Rat Hearts |
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卷期 | 32:5 |
作者 | Jia-Ping Wu 、 Shu Nu Chang-Lee 、 Cecilia Hsuan Day 、 Tsung-Jung Ho 、 Vijaya Padma Viswanadha 、 Li-Chin Chung 、 Jin-Ming Hwang 、 Gwo-Ping Jong 、 Wei-Wen Kuo 、 Chih-Yang Huang |
頁次 | 594-603 |
關鍵字 | Aging 、 Basic fibroblast growth factors 、 Connective tissue growth factor 、 Extracellularmatrix 、 Secondhand smoke exposure 、 MEDLINE 、 SCI 、 Scopus |
出刊日期 | 201609 |
DOI | 10.6515/ACS20150824C |
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 lowrate. Rats were exposed to SHS for 30min, 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 TGF1/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 TGF1/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. TGF1/p-Smad2/3/CTGF and FGF-2/UPA protein expression from SHS exposure were higher than that from aging. In contrast, MMP2 and MMP9were increased in aging rats comparedwith 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.