摘要
目的:观察电针(EA)是否通过增加SOCS3表达抑制JAK1/STAT3信号通路激活改善慢性阻塞性肺疾病(COPD)肺部炎症。方法:将60只小鼠随机分为空白组、模型(COPD)组、COPD+EA组、COPD+si-SOCS3组、COPD+si-SOCS3 NC组、COPD+si-SOCS3+EA组,每组10只。香烟烟熏3个月复制小鼠COPD模型,造模结束后,COPD+si-SOCS3组、COPD+si-SOCS3+EA组小鼠经滴鼻给予肺部SOCS3 siRNA,COPD+si-SOCS3 NC组小鼠滴鼻给予SOCS3 siRNA NC,第一次给药SOCS3 siRNA 24 h后,COPD+EA组、COPD+si-SOCS3+EA组给予“肺俞”“足三里”EA治疗,隔日1次,30 min/次,共14 d。检测各组小鼠肺功能,HE染色观察小鼠肺组织病理变化;ELISA检测各组小鼠肺泡灌洗液中IL-6、TNF-α、IL-1β变化;Western blot检测SOCS3、JAK1、STAT3、p-JAK1、p-STAT3蛋白表达;RT-PCR检测SOCS3、JAK1、STAT3 mRNA表达。结果:与空白组相比,COPD组小鼠肺功能下降,肺泡壁增厚,组织间有充血和水肿,炎症因子IL-6、TNF-α、IL-1β显著增多,SOCS3蛋白表达减少,p-JAK1/JAK1、p-STAT3/STAT3显著升高,JAK1、STAT3 mRNA增多,SOCS3 mRNA减少(P<0.05);与COPD组比较,COPD+EA组以上指标均有所改善(P<0.05),COPD+si-SOCS3组以上指标均更严重(P<0.05),COPD+si-SOCS3+EA组较COPD+si-SOCS3组有所改善(P<0.05)。结论:EA可通过上调SOCS3表达抑制JAK1/STAT3信号通路过度激活,进而改善COPD小鼠肺部炎症。
Objective:To observe whether electroacupuncture(EA)can inhibit activation of JAK1/STAT3 signaling pathway and improve pulmonary inflammation in chronic obstructive pulmonary disease(COPD)by increasing expression of SOCS3.Methods:Atotal of 60 mice were randomly divided into normal group,model(COPD)group,COPD+EA group,COPD+si-SOCS3 group,COPD+si-SOCS3 NC group,COPD+si-SOCS3+EA group,with 10 mice in each group.Mice COPD model was replicated by simple cigarette smoking for three months.After modeling,SOCS3 siRNA was administered to lungs of mice in COPD+si-SOCS3 group and COPD+si-SOCS3+EA group,SOCS3 siRNA NC was administered to COPD+si-SOCS3 NC group.24 h after the first SOCS3 siRNA ad-ministration,mice in COPD+EA and COPD+si-SOCS3+EA groups were treated with EA in"Feishu"and"Zusanli",once every other day,30 min/times for 14 days.Lung function of mice in each group was detected;lung pathological changes were observed by HE staining;IL-6,IL-1βand TNF-αlevels in mice broncho alveolar lavage fluid were detected by ELISA;protein expressions of SOCS3,JAK1,STAT3,p-JAK1 and p-STAT3 were detected by Western blot;SOCS3,JAK1 and STAT3 mRNA were detected by RT-PCR.Results:Compared with normal group,mice in COPD group showed decreased lung function,thickened alveolar walls,congestion and edema between tissues,significantly increased levels of inflammatory cytokines IL-6,TNF-αand IL-1β,decreased SOCS3 protein expres-sion,p-JAK1/JAK1 and p-STAT3/STAT3 significantly increased,JAK1 and STAT3 mRNA increased,SOCS3 mRNA decreased(P<0.05).Compared with COPD group,the above indexes of COPD+EA group were improved(P<0.05),and the above indexes of COPD+si-SOCS3 group were more serious(P<0.05),and COPD+si-SOCS3+EA group was improved compared with COPD+si-SOCS3 group(P<0.05).Conclusion:EA can inhibit overactivation of JAK1/STAT3 signaling pathway by up-regulating SOCS3 expression,and thus improve pulmonary inflammation in COPD.
作者
吴慧慧
潘祝
刘海燕
徐淑文
刘文美
张玉洁
刘自兵
WU Huihui;PAN Zhu;LIU Haiyan;XU Shuwen;LIU Wenmei;ZHANG Yujie;LIU Zibing(College of Acu-Moxibustion and Massage,Anhui University of Chinese Medicine,Hefei 230038,China)
出处
《中国免疫学杂志》
北大核心
2025年第8期1859-1864,共6页
Chinese Journal of Immunology
基金
安徽省高校自然科学基金重点项目(KJ2021A0569)
安徽省自然科学基金面上项目(2008085MH267)。
