p38蛋白激酶抑制剂SB239063对TNF-α介导支气管平滑肌收缩性增强的影响

Effect of p38 MAPK inhibitor SB239063 on TNF-α mediated enhanced bronchial smooth muscle contractility

目的研究p38MAPK抑制剂SB239063对TNF-α介导的支气管平滑肌收缩性增强的影响。方法显微镜下分离C57/BL6小鼠的支气管,并随机分为空白对照组、TNF-α处理组、TNF-α+p38MAPK抑制剂处理组,培养24小时后,利用肌动描记技术检测5-羟色胺(5-HT)、乙酰胆碱(ACh)诱导的支气管平滑肌等长收缩张力,比较预测收缩张力最大值(Emax)、产生50%最大收缩张力激动剂有效浓度的负对数(pEC50)。结果空白对照组、TNF-α+SB239063处理组5-HT、ACh诱导Emax小于TNF-α组。TNF-α+SB239063处理组对ACh诱导的收缩反应的pEC50小于TNF-α组。空白对照组与TNF-α+SB239063处理组之间Emax无差别,pEC50无差别。结论 p38MAPK抑制剂可抑制TNF-α介导支气管平滑肌对5-羟色胺、乙酰胆碱的收缩性增强。

Objective To investigate the effect of p38 MAPK inhibitor SB239063 on TNF-αmediated enhanced bronchial smooth muscle contractility.Methods The bronchi were isolated from C57/BL6 mice under the microscope and randomly divided into blank control group,TNF-αtreatment group,TNF-α＋p38 MAPK inhibitor SB239063 treatment group.The isometric contractile tension induced by 5-hydroxytryptamine（5-HT）and acetycholine（ACh）was recorded after 24 hours of culture using myograph.The estimated maximal isometric contractile tension（Emax）and negative logarithm of the agonist concentration that produces 50%of the maximal effect（pEC 50）were compared.Results The Emax induced by 5-HT and ACh from bronchi in the blank control group and the TNF-α＋SB239063 treatment group was less than the TNF-αtreatment group,the pEC 50from ACh induced contraction in the TNF-α＋SB239063 treatment group was less than the TNF-αtreatment group.The Emax and pEC50 induced by 5-HT and ACh between the blank control group and TNF-α＋ SB239063 treatment group was not different.Conclusionp38 MAPK inhibitor could inhibit the enhanced contractility of bronchial smooth muscle induced by 5-HT and ACh which is mediated by TNF-α.