[PDF][PDF] Non-steroidal anti-inflammatory drugs attenuate hyperalgesia and block upregulation of trigeminal ganglionic sodium channel 1.7 after induction of …

BI Rui Yun, Y Ding, YH Gan - Chin J Dent Res, 2016 - cjdrcsa.com
Objective: To investigate the association between the analgesic effect of non-steroidal
antiinflammatory drugs (NSAIDs) and sodium channel 1.7 (Nav1. 7) expression in the …

Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats

RY Bi, XX Kou, Z Meng, XD Wang… - European Journal of …, 2013 - Wiley Online Library
Background Inflammation is a major cause of temporomandibular disorder‐related pain. The
N av1. 7 sodium channel has a critical function in pain perceptions. However, whether and …

Progesterone attenuates allodynia of inflamed temporomandibular joint through modulating voltage‐gated sodium channel 1.7 in trigeminal ganglion

RY Bi, XY Zhang, P Zhang, Y Ding… - Pain Research and …, 2020 - Wiley Online Library
Background. Women with temporomandibular disorders (TMDs) experience some
amelioration of pain during pregnancy. Progesterone increases dramatically and steadily …

Prostaglandin E2 Upregulated Trigeminal Ganglionic Sodium Channel 1.7 Involving Temporomandibular Joint Inflammatory Pain in Rats

P Zhang, YH Gan - Inflammation, 2017 - Springer
Abstract Prostaglandin E 2 (PGE 2) is a key proinflammatory mediator that contributes to
inflammatory hyperalgesia. Voltage-gated sodium channel 1.7 (Na v 1.7) plays an important …

Glial interleukin-1β upregulates neuronal sodium channel 1.7 in trigeminal ganglion contributing to temporomandibular joint inflammatory hypernociception in rats

P Zhang, RY Bi, YH Gan - Journal of neuroinflammation, 2018 - Springer
Background The proinflammatory cytokine interleukin-1β (IL-1β) drives pain by inducing the
expression of inflammatory mediators; however, its ability to regulate sodium channel 1.7 …

Estradiol upregulates voltage-gated sodium channel 1.7 in trigeminal ganglion contributing to hyperalgesia of inflamed TMJ

RY Bi, Z Meng, P Zhang, XD Wang, Y Ding, YH Gan - PLoS One, 2017 - journals.plos.org
Background Temporomandibular disorders (TMDs) have the highest prevalence in women
of reproductive age. The role of estrogen in TMDs and especially in TMDs related pain is not …

Connexin 43 contributes to temporomandibular joint inflammation induced-hypernociception via sodium channel 1.7 in trigeminal ganglion

YZ Jin, P Zhang, T Hao, LM Wang, MD Guo… - Neuroscience Letters, 2019 - Elsevier
We previously demonstrated that sodium channel 1.7 (Nav1. 7) in trigeminal ganglion (TG)
was a critical factor in temporomandibular joint (TMJ) inflammation-induced …

Activation of voltage-gated KCNQ/Kv7 channels by anticonvulsant retigabine attenuates mechanical allodynia of inflammatory temporomandibular joint in rats

W Xu, Y Wu, Y Bi, L Tan, Y Gan, KW Wang - Molecular pain, 2010 - journals.sagepub.com
Background: Temporomandibular disorders (TMDs) are characterized by persistent orofacial
pain and have diverse etiologic factors that are not well understood. It is thought that central …

A new hypothesis of sex-differences in temporomandibular disorders: estrogen enhances hyperalgesia of inflamed TMJ through modulating voltage-gated sodium …

RY Bi, Y Ding, YH Gan - Medical hypotheses, 2015 - Elsevier
Objective: Temporomandibular disorders (TMD) are an assorted set of clinical conditions
characterized mainly by pain in the temporomandibular joint (TMJ). TMJ inflammation or …

[HTML][HTML] Inhibition of the Nav1. 7 channel in the trigeminal ganglion relieves pulpitis inflammatory pain

M Kwon, IY Jung, M Cha, BH Lee - Frontiers in pharmacology, 2021 - frontiersin.org
Pulpitis causes significant changes in the peripheral nervous system, which induce
hyperalgesia. However, the relationship between neuronal activity and Nav1. 7 expression …