香烟烟雾水提取物诱导大鼠支气管平滑肌收缩力增强

Q3 Medicine Journal of Smooth Muscle Research Pub Date : 2014-01-01
Hiroyasu Sakai, Ayako Watanabe, Akiko Fujita, Miwa Misawa, Minoru Narita, Yoshihiko Chiba
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引用次数: 0

摘要

吸烟是慢性阻塞性肺病(COPD)发病的主要风险因素。然而,人们对香烟烟雾诱导支气管平滑肌(BSM)高反应性的机制知之甚少。在本研究中,我们探讨了香烟烟雾水提取物(ACSE)对大鼠支气管平滑肌收缩的影响。与对照组相比,ACSE处理组的乙酰胆碱(ACh)、高K(+)去极化和氟化钠(NaF)诱导的BSM收缩显著增强。在 ACSE 处理的 BSM 中,肌球蛋白轻链激酶(MLCK)和 RhoA 的表达水平均明显增加。这些研究结果表明,香烟烟雾中的水溶性成分可能会通过增加 MLCK 和 RhoA 来引起 BSM 的高反应性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Augmented bronchial smooth muscle contractility induced by aqueous cigarette smoke extract in rats.

Cigarette smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD). However, little is known about the mechanisms of cigarette smoke-induced bronchial smooth muscle (BSM) hyperresponsiveness. In the present study, we investigated the effects of aqueous cigarette smoke extract (ACSE) on the BSM contraction in rats. The bronchial strips of rats were incubated with ACSE or control-extract for 24 h. The acetylcholine (ACh), high K(+) depolarization and sodium fluoride (NaF)-induced BSM contraction of the ACSE-treated group was significantly augmented as compared to that of the control one. The expression levels of both myosin light-chain kinase (MLCK) and RhoA were significantly increased in the ACSE-treated BSM. These findings suggest that the water-soluble components of cigarette smoke may cause BSM hyperresponsiveness via an increase in MLCK and RhoA.

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来源期刊
Journal of Smooth Muscle Research
Journal of Smooth Muscle Research Biochemistry, Genetics and Molecular Biology-Physiology
CiteScore
2.30
自引率
0.00%
发文量
7
审稿时长
10 weeks
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