清燥救肺汤及其分解剂对肺炎支原体感染小鼠TLR-2/NF-κB信号通路的影响  

Influence of Qingzao Jiufei decoction and its decomposable agent on TLR-2/NF-κB signal pathway in MP infected mice

作　　者：吴振起[1] 贾晓儒 敏娜 岳志军[1] 王雪峰[1] 张聪聪 WU Zhenqi;JIA Xiaoru;MIN Na;YUE Zhijun;WANG Xuefeng;ZHANG Congcong(Affiliated Hospital of Liaoning University of TCM,Shenyang 110032,China)

机构地区：[1]辽宁中医药大学附属医院儿科,沈阳110032 [2]辽宁中医药大学,沈阳110032

出　　处：《中国中西医结合儿科学》2017年第6期466-471,共6页Chinese Pediatrics of Integrated Traditional and Western Medicine

基　　金：国家自然科学基金面上项目(81373687);辽宁省科技厅项目(2014020044)

摘　　要：目的观察清燥救肺汤及其分解剂对肺炎支原体(MP)感染小鼠Toll样受体2(TLR-2)、髓样分化因子88(MyD88)、核因子κB(NF-κB)信号通路的影响,探讨其抗MP的作用机制。方法选择SPF级BALB/c小鼠144只,随机分成正常组、模型组、全方组、分解剂Ⅰ组、分解剂Ⅱ组及阿奇霉素组,每组24只。除正常组其他各组制备MP感染模型,造模成功后予药物灌胃治疗,并于感染后第3、7、10、14天进行取材。采用苏木精-伊红染色观察肺脏病理组织学改变、qPCR方法检测肺组织中TLR-2 mRNA变化、ELISA法检测血清中MyD88、TNF-α的含量及Western blot法检测肺组织NF-κB的表达。结果 MP感染后小鼠肺组织出现间质性炎症改变,7d时炎症最明显,14d时炎症逐渐减轻;治疗后各组肺部炎症均有改善,尤以第10、14天全方组、阿奇霉素组明显。MP感染后小鼠肺组织中TLR-2、NF-κB表达水平升高,血清中MyD88、TNF-α含量亦升高(P<0.05),各项指标出现峰值的时间不一致,其中NF-κB出现最早(第3天),TLR-2、TNF-α于第7天达峰值,而MyD88则相对较晚,于第10天达峰值。第7天,全方组即起效(P<0.05),肺组织中TLR-2、NF-κB表达水平下降,血清中MyD88、TNF-α含量亦降低;分解剂Ⅰ组在第10、14天亦能发挥类似全方组的作用,但较全方组偏弱(P>0.05);分解剂Ⅱ组在第14天TLR-2mRNA表达略升高。结论清燥救肺汤抗MP感染的机制与减少促炎因子的释放,调控TLR-2/NF-κB信号通路传导有关,其中分解剂Ⅰ起主要作用。ObjectiveTo observe the effect of Qingzao Jiufei decoction(QJD)and its decomposable agent on the toll like receptors(TLR)2/myeloid differentiation primary response gene88(MyD88)/(NF-κB)signal pathway in MP infected mice,and to explore its mechanism of action of resistance to MP.MethodsTotally144BALB/c mice,about20g in weight,were randomly divided into normal group(A),model group(B),QJD group(C),QJD decomposable agentⅠgroup(D),QJD decomposable agentⅡgroup(E)and azithromycin group(F),with24mice in each group.Each treatment group was made into MP infection model and the corresponding group was given corresponding drugs by intragastric administration after modeling.The serum and the lung tissues were detected after3,7,10and14days of MP infection.HE staining was used to observe the pathological change of lung tissues,qPCR was used to detect the changes of TLR-2mRNA in lung tissues,ELISA was used to detect the expressions of MyD88and TNFαin serum,and Western blot was used to detect the expression levels of NFκB in lung tissues.ResultsThe interstitial inflammatory changes of lung occurred3d after MP infection,which were most significant on the7d,and then gradually became less and less significant.Pulmonary inflammation in each treatment group was improved,especially in Group C and Group F on the10d and14d.The expression level of TLR-2and NF-κB in the lung tissue of mice after MP infection increased,and the content of MyD88and TNFαin serum was also increased(P<0.05).The peak time of each indicator was different with NFκB appearing earliest(3rd day),TLR-2and TNF-αpeaking on the7th day,while MyD88was relatively late,peaking on the10th day.On the7th day in Group C(P<0.05),the expression level of TLR-2and NF-κB in lung tissue decreased,and the content of MyD88and TNFαin serum was also decreased.Group D also played a similar role to Group C on the10th day and14th days,but weaker than Group C(P>0.05);in Group E on the14th day TLR-2mRNA expression slightly increased.ConclusionThe mechanism of QJD against MP infecti

关 键 词：肺炎支原体 清燥救肺汤 TLR-2/NF-κB信号通路 小鼠 

分 类 号：R332[医药卫生—人体生理学]