首页> 外文期刊>Life sciences >The involvement of TRPA1 channel activation in the inflammatory response evoked by topical application of cinnamaldehyde to mice.
【24h】

The involvement of TRPA1 channel activation in the inflammatory response evoked by topical application of cinnamaldehyde to mice.

机译:TRPA1通道激活参与局部应用肉桂醛对小鼠引起的炎症反应。

获取原文
获取原文并翻译 | 示例
           

摘要

AIMS: In the present work, we characterize the inflammatory process induced by the topical application of cinnamaldehyde on the skin of mice and verify the participation of transient receptor potential A1 TRPA1 receptors in this process. MAIN METHODS: We measured mouse ear edema and sensitization/desensitization after topical application of cinnamaldehyde or/and capsaicin. We also quantified cellular infiltration through myeloperoxidase (MPO) activity and histological and immunohistochemical analyses and evaluated the expression of TRPV1 and TRPA1 by western blot. KEY FINDINGS: Cinnamaldehyde induced ear edema in mice (1-6mug/ear) with a maximum effect of 4mug/ear. Cinnamaldehyde promoted leukocyte infiltration as detected by increasing MPO activity and confirmed by histological analyses. The edema and cellular infiltration evoked by the application of 4mug/ear of cinnamaldehyde were prevented by topical application of ruthenium red, a non-selective TRP antagonist as well as camphor and HC030031, two TRPA1 receptor antagonists. Cinnamaldehyde-induced edema, but not cellular infiltration, was prevented by topical application of the tachykinin NK1 antagonist, aprepitant, indicating a neuropeptide release phenomenon in this process. Additionally, we observed that repeated topical applications of cinnamaldehyde did not induce changes in sensitization or desensitization with respect to the edema response. Interestingly, repeated treatment with the TRPV1 agonist, capsaicin, abrogated it edematogenic response, confirming the desensitization process and partially decreasing the cinnamaldehyde-induced edema, suggesting the involvement of capsaicin-sensitive fibers. SIGNIFICANCE: Our data demonstrate that the topical application of cinnamaldehyde produces an inflammatory response that is dependent on TRPA1 receptor stimulation.
机译:目的:在目前的工作中,我们表征了肉桂醛在小鼠皮肤上局部应用诱导的炎症过程,并验证了瞬态受体电位A1 TRPA1受体在此过程中的参与。主要方法:我们测量了局部应用肉桂醛或/和辣椒素后的小鼠耳朵水肿和致敏/减敏作用。我们还通过髓过氧化物酶(MPO)活性以及组织学和免疫组化分析定量了细胞浸润,并通过Western印迹评估了TRPV1和TRPA1的表达。主要发现:肉桂醛可引起小鼠(1-6杯/耳)耳部水肿,最大作用为4杯/耳。肉桂醛通过增加MPO活性来检测并通过组织学分析证实了促进白细胞浸润。局部应用钌红(一种非选择性的TRP拮抗剂)以及樟脑和HC030031(两种TRPA1受体拮抗剂)可预防4杯/耳肉桂醛引起的水肿和细胞浸润。局部应用速激肽NK1拮抗剂阿瑞匹坦可预防肉桂醛引起的水肿,但不能阻止细胞浸润,表明在此过程中存在神经肽释放现象。此外,我们观察到肉桂醛的反复局部应用并未引起对水肿反应的敏化或脱敏改变。有趣的是,用TRPV1激动剂辣椒素进行的重复治疗消除了其致水肿反应,从而确认了脱敏过程并部分减少了由肉桂醛引起的水肿,表明辣椒素敏感纤维的参与。意义:我们的数据表明肉桂醛的局部应用可产生依赖于TRPA1受体刺激的炎症反应。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号