眼窩下神経慢性絞扼モデルマウスに対する神経傷害部位へのHMGB1中和抗体投与は三叉神経領域における疼痛様行動を抑制する

Trigeminal neuropathy, caused by injury to trigeminal nerve, manifests as orofacial numbness, paresthesias, or/and pain and are refractory to treatment with commonly used analgesics. In this study, we employed distal infraorbital nerve chronic constriction injury (dIoN-CCI) model, which mimic pathol...

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Bibliographic Details
Published in日本薬理学会年会要旨集 p. 1-P-017
Main Authors 河内, 貴弘, 中村, 庸輝, 中島, 一恵, 劉, 克約, 和氣, 秀徳, 西堀, 正洋, 入舩, 正浩, 森岡, 徳光
Format Journal Article
LanguageJapanese
Published 公益社団法人 日本薬理学会 2020
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Summary:Trigeminal neuropathy, caused by injury to trigeminal nerve, manifests as orofacial numbness, paresthesias, or/and pain and are refractory to treatment with commonly used analgesics. In this study, we employed distal infraorbital nerve chronic constriction injury (dIoN-CCI) model, which mimic pathology of trigeminal neuropathy, to investigate whether high mobility group box 1 (HMGB1), a kind of damage-associated molecular patterns, is involved in trigeminal neuropathy.Under anesthesia, silk sutures were tied loosely around the dIoN of ddY male mice. Nociceptive-like behaviors were evaluated by measurement of face grooming episodes and conditioned place preference test. Microglial activity in spinal trigeminal nucleus caudalis (Sp5c) was determined by immunohistochemistry. Anti-HMGB1 neutralizing antibody (nAb) was perineurally injected right after surgery.In dIoN-CCI mice, the mouse face grooming time was increased compared with sham mice. In addition, dIoN-CCI evoked activation of microglia in Sp5c and preference to mirogabalin-paired chamber. Moreover, the perineural treatment with anti-HMGB1 nAb blocked the dIoN-CCI-induced face grooming, microglia activation, and preference to mirogabalin. The anti-HMGB1 nAb could be a novel therapeutic reagent for inhibiting the induction of trigeminal neuropathy.
Bibliography:93_1-P-017
ISSN:2435-4953
DOI:10.1254/jpssuppl.93.0_1-P-017