Resveratrol inhibits mucus overproduction and MUC5AC expression in a murine model of asthma

被引:54
作者
Ni, Zhen-Hua [1 ]
Tang, Ji-Hong [2 ]
Chen, Guo [2 ]
Lai, Yi-Min [2 ]
Chen, Qing-Ge [2 ]
Li, Zao [2 ]
Yang, Wei [2 ]
Luo, Xu-Min [2 ]
Wang, Xiong-Biao [2 ]
机构
[1] Shanghai Univ Tradit Chinese Med, Putuo Hosp, Cent Lab, Shanghai 200062, Peoples R China
[2] Shanghai Univ Tradit Chinese Med, Putuo Hosp, Dept Resp Med, Shanghai 200062, Peoples R China
关键词
resveratrol; asthma; mucosal; mucin; 5AC; murine CLCA3; human CLCA1; AIRWAY INFLAMMATION; PREVALENCE;
D O I
10.3892/mmr.2015.4520
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Previous in vitro studies have demonstrated that resveratrol is able to significantly inhibit the upregulation of mucin SAC (MUC5AC), a major component of mucus; thus indicating that resveratrol may have potential in regulating mucus overproduction. However, there have been few studies regarding the resveratrol-mediated prevention of MUC5AC overproduction in vivo, and the mechanisms by which resveratrol regulates MUC5AC expression have yet to be elucidated. In the present study, an ovalbumin (OVA)-challenged murine model of asthma was used to assess the effects of resveratrol treatment on mucus production in vivo. The results demonstrated that resveratrol significantly inhibited OVA-induced airway inflammation and mucus production. In addition, the mRNA and protein expression levels of MUC5AC were increased in the OVA-challenged mice, whereas treatment with resveratrol significantly inhibited this effect. The expression levels of murine calcium-activated chloride channel (mCLCA)3, an important key mediator of MUC5AC production, were also reduced following resveratrol treatment. Furthermore, in vitro studies demonstrated that resveratrol significantly inhibited human (h)CLCA1 and MUC5AC expression in a dose-dependent manner. These results indicated that resveratrol was effective in preventing mucus overproduction and MUC5AC expression in vivo, and its underlying mechanism may be associated with regulation of the mCLCA3/hCLCA1 signaling pathway.
引用
收藏
页码:287 / 294
页数:8
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