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Involvement of TRPA1 in the cinnamaldehyde-induced pulpal blood flow change in the feline dental pulp

OBJECTIVES: The purpose of this study was to investigate the involvement of TRPA1 in the cinnamaldehyde-induced pulpal blood flow (PBF) change in the feline dental pulp. MATERIALS AND METHODS: Mandibles of eight cats were immobilized and PBF was monitored with a laser Doppler flowmetry at the mandib...

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Detalles Bibliográficos
Autores principales: Kim, Dokyung, Lee, Moon-Hwan, Kim, Sung Kyo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Academy of Conservative Dentistry 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4977351/
https://www.ncbi.nlm.nih.gov/pubmed/27508162
http://dx.doi.org/10.5395/rde.2016.41.3.202
Descripción
Sumario:OBJECTIVES: The purpose of this study was to investigate the involvement of TRPA1 in the cinnamaldehyde-induced pulpal blood flow (PBF) change in the feline dental pulp. MATERIALS AND METHODS: Mandibles of eight cats were immobilized and PBF was monitored with a laser Doppler flowmetry at the mandibular canine tooth. To evaluate the effect of cinnamaldehyde on PBF, cinnamaldehyde was injected into the pulp through the lingual artery at a constant rate for 60 seconds. As a control, a mixture of 70% ethanol and 30% dimethyl sulfoxide (DMSO, vehicle) was used. To evaluate the involvement of transient receptor potential ankyrin 1 (TRPA1) in PBF change, AP18, a specific TRPA1 antagonist, was applied into the pulp through the Class V dentinal cavity followed by cinnamaldehyde-administration 3 minutes later. The paired variables of experimental data were statistically analyzed using paired t-test. A p value of less than 0.05 was considered as statistically significant. RESULTS: Administration of cinnamaldehyde (0.5 mg/kg, intra-arterial [i.a.]) induced significant increases in PBF (p < 0.05). While administration of a TRPA1 antagonist, AP18 (2.5 - 3.0 mM, into the dentinal cavity [i.c.]) caused insignificant change of PBF (p > 0.05), administration of cinnamaldehyde (0.5 mg/kg, i.a.) following the application of AP18 (2.5 - 3.0 mM, i.c.) resulted in an attenuation of PBF increase from the control level (p < 0.05). As a result, a TRPA1 antagonist, AP18 effectively inhibited the vasodilative effect of cinnamaldehyde (p < 0.05). CONCLUSIONS: The result of the present study provided a functional evidence that TRPA1 is involved in the mechanism of cinnamaldehyde-induced vasodilation in the feline dental pulp.