文献类型：期刊文献

英文题名：Inhibition of airway remodeling and inflammation by isoforskolin in PDGF-induced rat ASMCs and OVA-induced rat asthma model

作者：Liang, Xin[1,2];Wang, Jingjing[1,2];Chen, Weiwei[1,2];Ma, Xiaoying[1,2];Wang, Yaqin[3];Nagao, Norio[4];Weng, Weiyu[1,2];Huang, Jianming[3];Liu, Jianwen[1,2]

机构：[1]East China Univ Sci & Technol, Sch Pharm, State Key Lab Bioreactor Engn, 130 Meilong Rd, Shanghai 200237, Peoples R China;[2]East China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab New Drug Design, 130 Meilong Rd, Shanghai 200237, Peoples R China;[3]Fudan Univ, Sch Pharm, 826 Zhangheng Rd, Shanghai 201203, Peoples R China;[4]Prefectural Univ Hiroshima, Dept Life & Environm Sci, Shobara 7270023, Japan

年份：2017

卷号：95

起止页码：275

外文期刊名：BIOMEDICINE & PHARMACOTHERAPY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000417744400034)】；

基金：Financial support from the Science and Technology Commission of the Shanghai Municipality (13401900502) and the Shanghai Committee of Science and Technology [grant 11DZ2260600] is gratefully acknowledged.

语种：英文

外文关键词：Isoforskolin; Airway remodeling; Airway inflammation; TGF-beta 1; IL-10/IL-1 beta

摘要：Isoforskolin (ISOF) has been reported to play an important role in many illnesses including respiratory, cardiovascular and ophthalmologic diseases. In our study, we aimed to investigate how ISOF regulates airway remodeling and inflammation in asthma. Based on SO2-stimulated mouse cough model, we assessed the role of ISOF in cough and secretion of phlegm. Afterwards, platelet derived growth factor (PDGF)-induced primary rat airway smooth muscle cell (ASMC) model and ovalbumin (OVA)-induced rat asthma model were used to continue our following research. Our results showed that ISOF could prolong the cough latent period, reduce the cough times in two minutes, and increase the excretion of red phenol, which suggested the antitussive and expectorant effects of ISOF. Besides, ISOF pretreatment reversed the hypotonicity and cytoskeleton remodeling in PDGF-induced ASMCs, and reduced mucus hypersecretion and collagen overdeposition in OVA-induced rat asthma model, which indicated its inhibition on airway remodeling in vitro and in vivo. Moreover, ISOF reduced the invasion of inflammatory cells into bronchoalveolar lavage fluid (BALF) and lungs, which revealed its inhibitory role in airway inflammation. The down-regulation of transforming growth factor beta 1 (TGF-beta 1) and interleukin-1 beta (IL-1 beta) upon ISOF treatment might be responsible for its anti-remodeling and anti-inflammation roles. In conclusion, ISOF can reduce cough and sputum, as well as inhibit airway remodeling and inflammation by regulating the expression of TGF-beta 1 and IL-1 beta. These data indicate the potency of ISOF in treating asthma and also provide insights into the development of new anti-asthma agent.