The involvement of TRPA1 channel activation in the inflammatory response evoked by topical application of cinnamaldehyde to mice |
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Authors: | Silva Cássia Regina Oliveira Sara Marchesan Rossato Mateus Fortes Dalmolin Gerusa Duarte Guerra Gustavo Petri da Silveira Prudente Arthur Cabrini Daniela Almeida Otuki Michel Fleith André Eunice Ferreira Juliano |
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Institution: | 1. Programa de Pós-graduação em Ciências Biológicas, Bioquímica Toxicológica, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil;2. Programa de Pós-graduação em Farmacologia Bioquímica e Molecular, UFMG, Belo Horizonte, MG, Brazil;3. Departamento de Farmacologia, Universidade Federal do Paraná, Curitiba, PR, Brazil;4. Departamento de Ciências Farmacêuticas, Universidade Estadual de Ponta Grossa, Ponta Grossa, PR, Brazil;5. Departamento de Biofísica e Farmacologia, Universidade Federal do Rio Grande do Norte, Natal, RN, Brazil |
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Abstract: | AimsIn 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 methodsWe 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 findingsCinnamaldehyde induced ear edema in mice (1–6 μg/ear) with a maximum effect of 4 μg/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 4 μg/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.SignificanceOur data demonstrate that the topical application of cinnamaldehyde produces an inflammatory response that is dependent on TRPA1 receptor stimulation. |
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