The mechanism of IL-1β contributing to temporomandibular joint inflammatory pain in rats

doi:10.19438/j.cjoms.2020.05.004

Abstract

Abstract: PURPOSE: To investigate whether the ERK1/2 and NF-κB signaling pathways are involved in interleukin-1beta (IL-1β) up-regulation of Nav1.7 expression and then participate in temporomandibular joint (TMJ) inflammatory pain in rats. METHODS: TMJ nociception and the expressions of p-ERK1/2, p-p65, Nav1.7, COX-2, and p-CREB were evaluated after inducing of TMJ inflammation or microinjecting of IL-1β into the trigeminal ganglion (TG). Rats TG explants were treated with IL-1β with or without inhibitors, including U0126 for ERK and PDTC for NF-κB, and then the gene expressions were evaluated using real-time PCR and Western blot assays. Statistical analysis was performed using SPSS 22.0 software package. RESULTS: TMJ inflammation or microinjection of IL-1β into the TG for 24 h both induced TMJ pain and correspondingly up-regulated p-ERK1/2, p-p65, Nav1.7, COX-2, and p-CREB expressions. Both U0126 and PDTC blocked IL-1β up-regulation of Nav1.7, COX-2, p-CREB expressions in TG explants. CONCLUSIONS: IL-1β up-regulates Nav1.7 expression through ERK1/2 and NF-κB signaling pathways, and then contributes to TMJ inflammatory pain in rats.

Key words: IL-1β, ERK1/2, NF-κB, Nav1.7, Temporomandibular inflammatory pain

CLC Number:

R782.6

PAN Hong-xiang, SUN Wei, YUAN Rong-tao, ZHANG Peng, QIU Jian-zhong. The mechanism of IL-1β contributing to temporomandibular joint inflammatory pain in rats[J]. China Journal of Oral and Maxillofacial Surgery, 2020, 18(5): 401-406.

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