Herbal cake-partitioned moxibustion inhibits colonic autophagy in Crohn’s disease via signaling involving distinct classes of phosphatidylinositol 3-kinases  

作　　者：Shi-Yuan Wang Ji-Meng Zhao Ci-Li Zhou Han-Dan Zheng Yan Huang Min Zhao Zhi-Ying Zhang Lu-Yi Wu Huan-Gan Wu Hui-Rong Liu 

机构地区：[1]Key Laboratory of Acupuncture-Moxibustion and Immunology,Shanghai University of Traditional Chinese Medicine,Shanghai 201203,China [2]Shanghai Research Institute of Acupuncture and Meridian,Shanghai 200030,China

出　　处：《World Journal of Gastroenterology》2020年第39期5997-6014,共18页世界胃肠病学杂志（英文版）

基　　金：the Program of Shanghai Academic Research Leader,No.17XD1403400;National Natural Sciences Foundation of China,No.81574079 and No.81873374;Three-year Action Plan Project of Shanghai Traditional Chinese Medicine Development,No.ZY(2018-2020)-CCCX-2004-01;Chinese Medicine Inheritance and Innovation"100 Million"Talent Project,Qi Huang Scholar;Shanghai Rising-Star Program,No.16QA1403400.

摘　　要：BACKGROUND Autophagy is an evolutionarily conserved biological process in eukaryotic cells that involves lysosomal-mediated degradation and recycling of related cellular components.Recent studies have shown that autophagy plays an important role in the pathogenesis of Crohn’s disease(CD).Herbal cake-partitioned moxibustion(HM)has been historically practiced to treat CD.However,the mechanism by which HM regulates colonic autophagy in CD remains unclear.AIM To observe whether HM can alleviate CD by regulating colonic autophagy and to elucidate the underlying mechanism.METHODS Rats were randomly divided into a normal control(NC)group,a CD group,an HM group,an insulin+CD(I+CD)group,an insulin+HM(I+HM)group,a rapamycin+CD(RA+CD)group,and a rapamycin+HM(RA+HM)group.2,4,6-trinitrobenzenesulfonic acid was administered to establish a CD model.The morphology of the colonic mucosa was observed by hematoxylin-eosin staining,and the formation of autophagosomes was observed by electron microscopy.The expression of autophagy marker microtubule-associated protein 1 light chain 3 beta(LC3B)was observed by immunofluorescence staining.Insulin and rapamycin were used to inhibit and activate colonic autophagy,respectively.The mRNA expression levels of phosphatidylinositol 3-kinase class I(PI3KC1),Akt1,LC3B,sequestosome 1(p62),and mammalian target of rapamycin(mTOR)were evaluated by RT-qPCR.The protein expression levels of interleukin 18(IL-18),tumor necrosis factor-α(TNF-α),nuclear factorκB/p65(NF-κB p65),LC3B,p62,coiled-coil myosin-like BCL2-interacting protein(Beclin-1),p-mTOR,PI3KC1,class III phosphatidylinositol 3-kinase(PI3KC3/Vps34),and p-Akt were evaluated by Western blot analysis.RESULTS Compared with the NC group,the CD group showed severe damage to colon tissues and higher expression levels of IL-18 and NF-κB p65 in colon tissues(P<0.01 for both).Compared with the CD group,the HM group showed significantly lower levels of these proteins(PIL-18<0.01 and Pp65<0.05).There were no significant differences in the expressio

关 键 词：Crohn’s disease Colon MOXIBUSTION MACROAUTOPHAGY Immunity Phosphatidylinositol 3-kinase signaling 

分 类 号：R245[医药卫生—针灸推拿学]