补肺益肾方对香烟烟雾提取物诱导的人支气管上皮细胞损伤的保护作用及其机制

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Protective effect of Bufei Yishen Formula against cigarette smoke extract-induced human bronchial epithelial cell damage and its mechanism

FANZhengyuan，2，3，SHENZihn，LI Ya，2，3 ，SHENTingting，2，3，LIGaofeng，LISuyu3

ChineseMedicineacoloyespiatorybotoryenanKeyLbatoryfditioalinsedicineforesptorisee PreventionandeatmentDepartmentofRespiratoryedicineistAfiliatedHospitalofHenanUnesityofineedicine Zhengzhou45OoChina;HenanProinceandMinistryofducationCo-constructionColaboratieInnoationCenterforCinese MedicineandRespiratoryiseases，HenanUniversityofhineseedicine，Zhengzhou45oo46，China

Abstract：ObjectiveToevaluatetheprotectiveefectofBufei YishenFormula （BYF）againstcigaretesmokeextract（CSE）- induced injuries inhuman bronchial epithelial BEAS-2Bcelsand explore theunderlying mechanism.MethodsBEAS-2Bcels exposed to CSE were treated with normal rat serum，BYF-medicated rat serum at low or high doses，pyrrlidine dithiocarbamate（DC，aNF-Bbitor），DTCombinedwithigh-dose-medicatedserum，orabomethyloteine （S-CMC，astheosiiecotrol）.CCK-8ssaysusedtoetemietheoialoncentratioandtreamenttieofCE，BmedicatedserumandS-CMC.Thetreatedcelswereexaminedforinflammatoryfactor levels inthesupernatantandcelular expresions ofMUC5ACandMUC5Busing ELISA，cellultrastructural changes withtransmision electron microscopyand cellapoptosisrateusingflowcyometry.TheexpressionlevelsofTR4/NF-Bpathway-ssiatedmRNAsandproteinswere determinedbyqRT-PCRandWesternbloting.ResultsCSEexposuresignificantlyincreasedsecretionsofIL-β，IL-6andNF α， mRNA and protein expresonsof MUC5ACand MUC5B，andearlyand totalapoptosisrates in BEAS-2Bcels， where the presence ofapoptoticbodies was detected.CSEalsosignificantlyenhanced themRNAand protein expresionsofTR4，I-kB， and NF-kB and reduced mRNA and protein expresions of AQP5. Treatments of the CSE-exposedcelswith BYF-medicated serum，PDCand-Callsigicatlyloweredinammatryactorlevels，UAandCBexpiosadearly andtotalcellapoptosisratesandpartlyeversedthechangesincellularultrastructureandmRAandproteiexpresiosof theTLR4/NF-Bpathwayandtheeffectswerethemostconspicuousfolowingthecombinedtreatmentwithig-doseBYmedicated serum and PDTC. Conclusion BYFcan inhibit cell apoptosis，inflammationand mucus hypersecretion in CSEinduced BEAS-2B cells by inhibiting the TLR4/NF-kB signaling pathway.

Keywords： inflammationresponse;cigaretesmokeextract;Bufei YishenFormula; mucin hypersecretion;TLR4/NF-Bsignaling pathway

慢性阻塞性肺疾病（COPD），是一种以持续且不可逆的气流受限为特征的慢性气道疾病，为全球第3大死亡原因，第7大致残疾病[2]。（剩余13148字）