哮喘大鼠Caveolin-1通过PI3K/AKT途径对气道重塑的影响  

Effect of Caveolin-1 via PI3K/AKT pathway on airway remodeling in asthmatic rat

作　　者：徐慧[1] 戴元荣[1] 李凤琴[1] 夏梦玲[1] 

机构地区：[1]浙江省温州医科大学附属第二医院呼吸科,325027

出　　处：《中华全科医学》2015年第6期890-892,1037,共3页Chinese Journal of General Practice

基　　金：浙江省温州市科技局项目(Y20130351);浙江省自然科学基金(Y2080466)

摘　　要：目的研究Caveolin-1通过PI3K/AKT途径对TGF-β1刺激引起的气道平滑肌细胞(airway smooth muscle cells,ASMCs)增殖的影响。方法 30只健康雄性SD大鼠随机分为正常对照组和哮喘组,每组15只,以卵白蛋白致敏和激发建立大鼠哮喘模型。ASMCs的培养和鉴定,并分为TGF-β1组、哮喘组、正常对照组、wortmannin+TGF-β1组、β-CD+TGF-β1组,用CCK-8法检测哮喘大鼠ASMCs的增殖,western blot法检测ASMCs上Caveolin-1、p-AKT的表达。结果 1TGF-β1组较正常对照组和哮喘组细胞增殖明显(P<0.01,P<0.05);wortmannin+TGF-β1组较TGF-β1组细胞增殖减少(P<0.01)。2ASMCs Caveolin-1的表达:哮喘组较正常对照组明显减少,TGF-β1组较哮喘组表达量减少(均P<0.01);3ASMCs p-AKT的表达:哮喘组p-AKT表达明显高于正常对照组,TGF-β1组则高于较哮喘组,wortmannin+TGF-β1组明显低于TGF-β1组,β-CD+TGF-β1组较TGF-β1组表达量增加(均P<0.01)。结论通过上调Caveolin-1表达、抑制PI3K活化可以抑制TGF-β1刺激导致的哮喘大鼠ASMCs的增殖。Objective To investigate the effect of Caveolin-1 on TGF-β1-induced airway smooth muscle ceils （ASMCs） proliferation via PI3K/AKT signaling pathway in asthmatic rats. Methods Thirty male adult Spragne-Dawley （SD） rats were randomly divided into the control group and the asthma group. The ovalbumin-induced asthma rat model was created. Rat ASMCs were cultured in vitro. The cells were divided into TGF-β1 group, asthma group, control group, wortmannin ＋ TGF-β1 group, β-CD ＋ TGF-β1 group. The proliferation of ceils was detected with CCK8 method. The expression of Caveo- lin-1 and p-AKT protein was detected with Western Blot method. Results ①The proliferation of ASMCs in TGF-β1 group increased significantly than control group and asthma group（ P 〈 0.01 ,P 〈 0.05 ）. While the ASMCs in the wort- mannin ＋ TGF-β1 group decreased significantly than TGF-β1 group（ P 〈 0.01 ）. ②The expression of Caveolin-1 in ASMCs of asthmatic group decreased significantly than the control group, and it in TGF-β1 group was less than asthma group （both P 〈 0.01 ）. ③The expression of p-AKT in ASMCs of asthma group increased significantly than control group, and it in TGF-β1 group was more than asthma group（ both P 〈 0.01 ）. While it in wortmannin ＋ TGF-β1 group was less than TGF- β1 group and it in β-CD ＋ TGF-β1 group was more than TGF-β1 group （ both P 〈 0.O1 ）. Conclusion Caveolin-1 can sup- press TGF-β1 -induced airway smooth muscle cells proliferation in asthmatic rats via PI3K/AKT signaling pathway.

关 键 词：微囊蛋白 磷脂酰肌醇3激酶 气道平滑肌细胞 

分 类 号：R562.25[医药卫生—呼吸系统] R332.3[医药卫生—内科学]