木姜子和忍冬藤“公药”、“母药”相配改善哮喘ASMC病变和气道重塑的机制研究

Bronchial asthma is one of common chronic diseases seriously threaten to health worldwidely. Recently researches indicated that airway remodeling had taken an important affection on the progress of asthma,and the pathologic changes of airway smooth muscle cell (ASMC) had played a key role on the occurrence of airway remodeling. Our research team has found that combination of ‘Male herb’Litsea cubeba (Lour.) Pers and ‘female herb’Lonicera Japonica Thunb could improve lung function and the expression of caspase-3 ,meantime,reduce the levels of NF-κB and IL-17 so that to inhibit the proliferation of ASMC and airway remodeling in the mice with asthma. Based on which , it was supposed that combination of ‘Male herb’Litsea cubeba (Lour.) Pers and ‘female herb’Lonicera Japonica Thunb could take an effect on the treatment of asthma by regulating the pathologic changes of ASMC,such as proliferation,apoptosis,inflammatory secrete so to inhibit airway remodeling . This project is aimed to investigate the mechanism of combination of ‘Male herb’Litsea cubeba (Lour.) Pers and ‘female herb’Lonicera Japonica Thunb improving pathologic changes of ASMC and airway remodeling .Our findings were expected to explain the scientific connotation about combination of ‘Male herb’ and ‘female herb’ in the theory of Zhuang nationality medicine ,to provide basic information for studies of component and efficacy of Zhuang nationality herbs and to find innovation for the treatment of asthma.

支气管哮喘是全世界范围内严重威胁人们健康的常见慢性病之一。近来研究表明气道重塑在哮喘的进展中有重要作用，气道平滑肌细胞病理变化在气道重塑的发生中扮演关键性角色，课题组前期工作显示壮药木姜子和忍冬藤 “公药”、“母药”配伍可改善哮喘小鼠的肺功能、凋亡蛋白caspase-3 表达，同时，降低炎症通路重要分子NF-κB和气道炎症细胞因子IL-17的水平，抑制气道平滑肌细胞的增殖。推测木姜子和忍冬藤配伍通过调节气道平滑肌增殖、凋亡、炎性分泌等病理变化，从而抑制气道重塑起到改善哮喘症状的作用。本课题在此基础上，从动物实验（整体水平）和细胞培养(细胞水平)开展研究，探讨木姜子和忍冬藤配伍调节气道平滑肌病理变化而抑制气道重塑达到治疗哮喘的机制，研究结果将揭示木姜子和忍冬藤 “公药”、“母药”配伍的科学内涵，为壮药“公药”、“母药”配伍理论和药效组分规律的研究提供基础资料，并为哮喘的治疗找到新的切入点。

支气管哮喘（简称哮喘）是全世界范围内严重威胁人们健康的常见慢性病之一。气道重塑在哮喘的进展中有重要作用，气道平滑肌细胞（ASMC）病理变化在气道重塑的发生中扮演关键性角色。壮药木姜子和忍冬藤 “公药”、“母药”配伍可改善哮喘症状，但其具体机制尚不明确。本项目建立哮喘小鼠动物模型和ASMC细胞培养模型，采用木姜子和忍冬藤 “公药”、“母药”配伍干预，检测相关指标，阐明木姜子和忍冬藤配伍改善哮喘的机制。本项目研究结果显示木姜子和忍冬藤配伍高剂量组IgE水平（29.36±7.55）、IL- 4水平（24.19±4.87）、IL-5水平（54.22±4.09）、IL-10水平（89.36±27.02）、IL-17水平（61.55±22.01）、VEGF水平（25.61±7.25）、PDGF水平（21.36±5.98）、STAT-6水平（56.39±15.61）、ERK1/2蛋白相对表达（0.18±0.02）、Bcl-2 蛋白相对表达（0.22±0.04）均显著下降而IFN-γ水平（34.01±1.96）、FAS蛋白相对表达（0.82±0.07）、0.1秒用力呼气容积（FEV0.1）（0.53±0.008）、0.2秒用力呼气容积（FEV0.2）（0.61±0.006）、第0.4秒用力呼气容积占用力肺活量比值（FEV0.4/FVC）（0.68±0.06）、呼气峰流速（PEF）（8.35±0.17）均显著升高，提示木姜子和忍冬藤配伍通过调节改善哮喘ASMC 增殖、凋亡及合成分泌功能等，降低哮喘炎症反应，从而抑制气道重塑达到缓解哮喘症状的具体起效机制，揭示木姜子和忍冬藤 “公药”、“母药”配伍治疗哮喘的科学内涵，项目研究为木姜子和忍冬藤配伍治疗哮喘的临床应用提供基础研究依据。