Cardio Protective Effects of Lumbrokinase and Dilong on Second-Hand Smoke-Induced Apoptotic Signaling in the Heart of a Rat Model

doi:10.4077/CJP.2015.BAD277

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Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/29733

Title:	Cardio Protective Effects of Lumbrokinase and Dilong on Second-Hand Smoke-Induced Apoptotic Signaling in the Heart of a Rat Model
Authors:	Liao, Hung-En Lai, Chao-Hung Ho, Tsung-Jung Yeh, Yu-Lan Jong, Gwo-Ping Kuo, Wu-Hsien Chung, Li-Chin Pai, Pei-ying Wen, Su-Ying Huang, Chih-Yang
Contributors:	醫務管理系
Keywords:	cardiac survival signaling caspases death-receptor-dependent pathway dilong lumbrokinase mitochondria-dependent pathway second-hand smoke (SHS)
Date:	2015-06
Issue Date:	2016-04-19 19:06:15 (UTC+8)
Publisher:	Chinese Physiological Soc
Abstract:	Exposure to second-hand tobacco smoke (SHS) has been epidemiologically linked to heart disease among non-smokers. However, the molecular mechanism behind SHS-induced cardiac disease is not well known. This study found that SD rats exposed to cigarette smoke at a dose of 10 cigarettes for 30 min twice a day for 1 month had a reduced left ventricle-to-tibia length ratio (mg/mm), increased cardiomyocyte apoptosis by TUNEL assay and a wider interstitial space by H&E staining. However, lumbrokinase and dilong both reversed the effects of SHS. Western blotting demonstrated significantly increased expression of the pro-apoptotic protein caspase-3 in the hearts of the rats exposed to SHS. Elevated protein expression levels of Fas, FADD and the apoptotic initiator activated caspase-8, a molecule in the death-receptor-dependent pathway, coupled with increased t-Bid and apoptotic initiator activated caspase-9 were found. Molecules in the mitochondria-dependent pathway, which disrupts mitochondrial membrane potential, were also found in rats exposed to SHS. These factors indicate myocardial apoptosis. However, treatment with lumbrokinase and dilong inhibited SHS-induced apoptosis. Regarding regulation of the survival pathway, we found in western blot analysis that cardiac protein expression of pAkt, Bcl2, and Bcl-xL was significantly down-regulated in rats exposed to SHS. These effects were reversed with lumbrokinase and dilong treatment. The effects of SIB on cardiomyocytes were also found to be mediated by the Fas death receptor-dependent apoptotic pathway, an unbalanced mitochondria membrane potential and decreased survival signaling. However, treatment with both lumbrokinase and dilong inhibited the effects of SITS. Our data suggest that lumbrokinase and dilong may prevent heart disease in SITS-exposed non-smokers
Relation:	Chinese Journal of Physiology, v.58 n.3, pp.188-196
Appears in Collections:	[Dept. of Hospital and Health (including master's program)] Periodical Articles

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