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[变应性鼻炎中p38丝裂原活化蛋白激酶对MUC5AC调控机制的初步研究]

[A preliminary study on the regulation mechanism of p38MAPK on MUC5AC in allergic rhinitis].

作者信息

Wang Zhenlin, Li Peng, Li Yuan, Zhang Qiuhang, Qu Qiuyi, Qi Yan

机构信息

Department of Otolaryngology--Head and Neck Surgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.

出版信息

Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2011 Oct;25(20):943-6.

Abstract

OBJECTIVE

To detect the effect of p38 mitogen activated protein kinase (p38MAPK) and cyclooxygenase-2 (COX-2) on the expression of mucin5AC (MUC5AC) in human nasal mucosa induced by histamine in vitro, and to investigate the pathogenesis of mucus hypersecretion in allergic rhinitis (AR).

METHOD

Western blot was performed to detect the protein expressions of p38MAPK, COX-2 and MUC5AC in nasal mucosa induced by histamine or blocked by selective inhibitors of p38MAPK and COX-2 of different concentration gradient.

RESULT

Weak expressions of p38MAPK. COX-2 and MUC5AC were detected in normal nasal mucosa in vitro. The protein expressions of p38MAPK. COX-2 and MUC5AC increased in nasal mucosa induced by histamine in a dose-dependent manner. The histamine induced protein expressions of COX-2 and MUC5AC were dose-dependently attenuated by selective inhibitor of COX-2, namely NS-398. No apparent influence of NS-398 on the expression of p38MAPK was observed. The histamine induced protein expressions of p38MAPK, C()X-2 and MUCbAC dose-dependently decreased after nasal mucosa was treated by selective inhibitor of p38MAPK, namely SB203580. And no significant change of MUC5AC protein expression induced by NS-398 or SB203580 was observed.

CONCLUSION

Our findings indicated that the histamine-induced increased expression of MUC5AC by activated p38MAPK/COX-2 may be a possible pathogenesis of mucus hypersecretion in AR.

摘要

目的

检测p38丝裂原活化蛋白激酶(p38MAPK)和环氧化酶-2(COX-2)对体外组胺诱导的人鼻黏膜黏蛋白5AC(MUC5AC)表达的影响,探讨变应性鼻炎(AR)中黏液高分泌的发病机制。

方法

采用蛋白质印迹法检测不同浓度梯度的组胺诱导或p38MAPK和COX-2选择性抑制剂阻断后的鼻黏膜中p38MAPK、COX-2和MUC5AC的蛋白表达。

结果

体外正常鼻黏膜中检测到p38MAPK、COX-2和MUC5AC的弱表达。组胺诱导的鼻黏膜中p38MAPK、COX-2和MUC5AC的蛋白表达呈剂量依赖性增加。COX-2选择性抑制剂NS-398可剂量依赖性减弱组胺诱导的COX-2和MUC5AC蛋白表达。未观察到NS-398对p38MAPK表达有明显影响。p38MAPK选择性抑制剂SB203580处理鼻黏膜后,组胺诱导的p38MAPK、COX-2和MUC5AC蛋白表达呈剂量依赖性降低。未观察到NS-398或SB203580诱导的MUC5AC蛋白表达有显著变化。

结论

我们的研究结果表明,组胺通过激活p38MAPK/COX-2诱导MUC5AC表达增加可能是AR中黏液高分泌的一种可能发病机制。

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