CAJ | 학술논문

目的观察熏烟对小鼠肺组织中Muc1表达的影响,并初步探讨其表达水平的改变与烟雾刺激的关系.方法 C57雄性小鼠随机分为熏烟组(8只)和对照组(8只),熏烟处理或正常饲养相同时间后处死小鼠,对支气管肺泡灌洗液(BALF)进行细胞计数、染色和分类,同时测定BALF中肿瘤坏死因子α(TNF-α)水平；通过酶联免疫吸附测定法及蛋白质免疫印迹法对BALF及肺组织中Muc1蛋白水平进行检测.同时对香烟烟雾提取物刺激肺上皮来源的A549细胞后MUC1的表达水平进行了验证.结果与对照组比较,熏烟组小鼠肺组织中出现明显炎症细胞浸润,BALF中的细胞总数、中性粒细胞数、巨噬细胞数均增高.同时,熏烟组小鼠的肺组织及BALF中的Muc1表达水平以及BALF中TNF-α的水平均高于对照组(P＜0.05或P＜0.01).此外,香烟烟雾提取物刺激A549细胞后,可诱导黏蛋白MUC1表达上升.结论熏烟可以导致小鼠肺组织炎症反应并伴随Muc1的表达水平升高和TNF-α 分泌的增加,MUC1表达水平的增加可能与香烟烟雾直接作用于肺上皮细胞有关.
목적 관찰훈연대소서폐조직중Muc1표체적영향,병초보탐토기표체수평적개변여연무자격적관계.방법 C57웅성소서수궤분위훈연조(8지)화대조조(8지),훈연처리혹정상사양상동시간후처사소서,대지기관폐포관세액(BALF)진행세포계수、염색화분류,동시측정BALF중종류배사인자α(TNF-α)수평；통과매련면역흡부측정법급단백질면역인적법대BALF급폐조직중Muc1단백수평진행검측.동시대향연연무제취물자격폐상피래원적A549세포후MUC1적표체수평진행료험증.결과 여대조조비교,훈연조소서폐조직중출현명현염증세포침윤,BALF중적세포총수、중성립세포수、거서세포수균증고.동시,훈연조소서적폐조직급BALF중적Muc1표체수평이급BALF중TNF-α적수평균고우대조조(P＜0.05혹P＜0.01).차외,향연연무제취물자격A549세포후,가유도점단백MUC1표체상승.결론 훈연가이도치소서폐조직염증반응병반수Muc1적표체수평승고화TNF-α 분비적증가,MUC1표체수평적증가가능여향연연무직접작용우폐상피세포유관.
Objective To observe the impacts of cigarette smoking on lung Muc1 expression and investigate the relationships between Muc1 changes and cigarette smoking stimulations in lung.Methods Male C57 mice were randomly divided into cigarette smoking group ( n =8) and normal control group ( n =8).After the cigarette smoke exposures or not,the mice were sacrificed and the total and differential cell numbers in bronchoalveolar lavage fluid (BALF) were counted.The level of tumor necrosis factor-α(TNF-α) in BALF was measured.The Muc1 level in BALF and lung was determined with ELISA and Western blot respectively.The lung Muc1 changes responded to cigarette smoke exposure were confirmed by detecting the MUC1 levels in cultured human lung epithelial A549 cells treated with cigarette smoke extract.Results The higher Muc1 level in lung and BALF was found in cigarette smoke exposed mice (P＜0.05),accompanied with increases on total cell numbers,neutrophils and macrophages numbers and the level of TNF-α in bronchoalveolar lavage fluid ( P＜0.05 or P＜0.01).Furthermore,the MUC1 level was upregulated in the cigarette smoke extract treated A549 cells.Conclusions Cigarette smoking induces lung inflammation with upregulations on MUC1 and TNF-α levels.The Muc1 increase might originate from the stimulation of cigarette smoke to the lung epithelial cells.