依卡倍特钠对反流性食管炎大鼠食管黏膜的保护作用及可能机制

Esophageal mucosa protective effects and its mechanism of Ecabet sodium in rat reflux esophagitis

目的:探讨依卡倍特钠(ES)对反流性食管炎大鼠食管黏膜病变的保护作用及其机制。方法:采用食管十二指肠吻合术建立大鼠RE模型,进行药物干预。HE染色检测各组大鼠食管黏膜损伤情况;ELISA检测各组大鼠血清炎症因子水平;Real-time PCR检测食管内TNFα、IL-1、Cox2mRNA表达;Western blot检测食管内ERK及P38通路活化。结果:ES低、中、高浓度干预不同程度缓解了食管黏膜病变,降低血清中TNFα、IL-1β水平及食管中TNFα、IL-1、Cox2表达(P<0.05),抑制ERK及P38通路的异常活化(P<0.05)。结论:ES通过抑制MAPK信号通路抑制TNFα、IL-1、Cox2的表达,影响炎症因子的释放和炎症发生,从而缓解食管黏膜病变。

Objective:To inquire into the esophageal mucosa protective effects of Ecabet sodium(ES)in rat reflux esophagitis(RE)and its possible mechanism.Methods:The operation of end-to-side anastomosis of the esophagus and duodenum was performed to establish rat RE model.Esophageal mucosa lesion was examined by HE stain.The level of TNFαand IL-1βin sera was determined by ELISA.The level of TNFα,IL-1and Cox2 in esophageal tissues were detected by Real-time PCR.The activation of ERK and P38 was detected by western blot.Results:Low,middle and high concentration ES intervention showed different levels of alleviation of esophageal mucosa disease,decreased the level of TNFαand IL-1βin serum and TNFα,IL-1,Cox2 in esophagus(P<0.05).Otherwise,ES inhibited the abnormality activation of ERK and P38(P<0.05).Conclusion:By inhibiting the MAPK signaling pathways and suppress the expression of TNFα,IL-1and Cox2,ES thereby inhibits the release of inflammatory cytokines and inflammation,and as a result reduces esophageal mucosal lesions in RE model.