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논문 기본 정보

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학술저널
저자정보
Myung-Dong Kim (Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu, Republic of Korea) Yu-Mi Kim (Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu, Republic of Korea) Jo-Young Son (Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu, Republic of Korea) Jin-Sook Ju (Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu, Republic of Korea) Dong-Kuk Ahn (Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu, Republic of Korea)
저널정보
조선대학교 치의학연구원 Oral Biology Research Oral Biology Research Vol.48 No.2
발행연도
2024.6
수록면
37 - 44 (8page)
DOI
10.21851/obr.48.02.202406.37

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The study aimed to investigate the role of peripheral NLR family pyrin domain-containing 3 protein (NLRP3) in inflammatory pain development in the orofacial area. Male Sprague–Dawley rats were used in experiments, with orofacial formalin-induced pain behavior and complete Freund’s adjuvant (CFA)-induced thermal hyperalgesia as chronic inflammatory pain models. Administration of 5% formalin produced biphasic nociceptive behavior, and subcutaneous pretreatment with MCC950 (50 and 100 μg/50 μL), an NLRP3 inhibitor, remarkably attenuated nociceptive behavior during the second phase. Subcutaneous CFA injection induced thermal hyperalgesia 1 day after injection, which persisted for 7 days. Five days after CFA injection, subcutaneous treatment with MCC950 (50 and 100 μg/50 μL) significantly attenuated thermal hyperalgesia. Additionally, subcutaneous injection of BMS-986299 (50 and 100 μg/50 μL), an NLRP3 agonist, induced significant nociceptive behavior for 1 hour in naïve rats. Pretreatment with an interleukin- 1β (IL-1β) receptor antagonist blocked the nociceptive behavior produced by subcutaneous injection of BMS-986299 (100 μg/50 μL); however, treatment with a hypoxia-inducible factor 1α inhibitor did not. These findings suggest the involvement of the peripheral NLRP3 and IL-1β pathway in chronic inflammatory pain development in the orofacial area, highlighting the potential of blocking this pathway as a strategy for developing future inflammatory pain treatment drugs.

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