黄芪多糖抑制气道平滑肌细胞α-SMA的表达  

Astragalus polysaccharides down-regulate expression of α-SMA in airway smooth muscle cells

作　　者：张学平[1] 王莉[1] 龙飞[1] 李怀臣[1] 

机构地区：[1]山东大学附属省立医院呼吸内科,济南250021

出　　处：《山东大学学报（医学版）》2011年第2期79-82,87,共5页Journal of Shandong University:Health Sciences

基　　金：山东省科技攻关计划资助项目(2007GG30002033)

摘　　要：目的研究黄芪多糖(APS)在支气管哮喘(哮喘)治疗中对气道平滑肌细胞α-平滑肌肌动蛋白(α-SMA)表达的影响及其作用机制。方法由膜荚黄芪提取APS,培养人气道平滑肌细胞系,设APS20、100、500μg/mL3种浓度组及对照组、脂多糖(LPS)组和Toll样受体4(TLR4)拮抗剂组,应用转化生长因子-β(TGF-β)诱导细胞α-SMA的高表达,细胞免疫化学染色、Western blot及PCR技术检测各组的α-SMA、mRNA水平。结果 APS中高浓度组可抑制气道平滑肌细胞α-SMA的高表达(P<0.01),降低α-SMA、mRNA水平(P<0.01),TLR4拮抗剂可部分抑制APS对α-SMA的作用(P<0.01)。结论 APS通过TLR4抑制由TGF-β诱导的气道平滑肌细胞α-SMA的高表达,这可能成为防治哮喘的新途径。Objective：To investigate the effect of astragalus polysaccharides（APS） on expression of α-smooth muscle actin（α-SMA） in airway smooth muscle cells,and to investigate the possible mechanism of the effect.Methods：APS were isolated from Astragalus membranaceus.Cultivated human airway smooth muscle cells were divided into the APS groups in doses of 20,100 and 500 μg/mL,the control group,the lipopolysaccharide（LPS） group and Toll-like receptor 4（TLR4） antagonist group,and subsequently stimulated to express α-SMA by TGF-β.Expressions of α-SMA and mRNA were measured by immunocytochemistry,Western blot and RT-PCR.Results：Medium and high concentrations of APS inhibited expression of α-SMA（P0.01） and down-regulated the level of α-SMA mRNA（P0.01）,which could be partly reversed by the TLR4 antagonist（P0.01）.Conclusion：APS down-regulates expression of α-SMA stimulated by TGF-β in airway smooth muscle cells through TLR4,and has a potential role in the prevention and treatment of asthma.

关 键 词：哮喘 肌动蛋白类 肌 平滑 黄芪属植物 TOLL样受体4 

分 类 号：R562.25[医药卫生—呼吸系统]