| Literature DB >> 24706507 |
Chao-Hung Lai1,2, Chien-Kuo Han3, Marthandam Asokan Shibu4, Pei Ying Pai5, Tsung-Jung Ho6,7, Cecilia Hsuan Day8, Fuu-Jen Tsai6, Chang-Hai Tsai9, Chun-Hsu Yao10, Chih-Yang Huang3,4,6.
Abstract
Exposure to tobacco smoke has epidemiologically been linked to the occurrence of cardiovascular disease among nonsmokers but the associated molecular events are not well elucidated yet. When Sprague Dawley rats were exposed to second-hand tobacco cigarette smoke twice a day for a 30 days period at an exposure rate of 10 cigarettes/30 min, they showed adverse effects including reduced left ventricle weight, increased cardiac damages, deteriorated cardiac features, and cardiac fibrosis. Exposure to second-hand smoking (SHS) increased the molecular markers of cardiac fibrosis such as urokinase plasminogen activator and matrix metallopeptidases. The modulations in the protein levels were led by the activation of extracellular signal-regulated kinases (ERK1/2), the transcription factor-specificity protein 1 (SP1), and the fibrogenic master switch-connective for epithelial-mesenchymal transition tissue growth factor there by indicating their effective role in SHS-induced myocardial infraction. Dilong, an edible earthworm extract used in Chinese medicine and its bioactive fibrinolytic enzyme product-lumbrokinase, when administered in rats, restricted the SHS exposure induced cardiac fibrosis and provided cardio-protection. The results show that lumbrokinase and dilong administration can efficiently prevent epidemiological incidence of cardiac disease among SHS-exposed nonsmokers.Entities:
Keywords: cardiac fibrosis; dilong; lumbrokinase; second-hand smoke
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Year: 2014 PMID: 24706507 DOI: 10.1002/tox.21993
Source DB: PubMed Journal: Environ Toxicol ISSN: 1520-4081 Impact factor: 4.119