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TRPV1 regulates inflammatory process in the tongue of surgically induced xerostomia mouse.

Authors
  • Yoo, Min H1
  • Rhee, Yun-Hee2, 3
  • Jung, JaeYun3, 4
  • Lee, Sang-Joon4
  • Moon, Jung-Hwan2, 3, 4
  • Mo, Ji-Hun2, 3, 4
  • Chung, Phil-Sang2, 3, 4
  • 1 Department of Innovative Toxicology Research, Korea Institute of Toxicology, Daejeon, Republic of Korea. , (North Korea)
  • 2 Laser Translational Clinical Trial Center, Dankook University Hospital, Cheonan, Republic of Korea. , (North Korea)
  • 3 Beckman Laser Institute Korea, Dankook University, Cheonan, Republic of Korea. , (North Korea)
  • 4 Department of Otorhinolaryngology, College of Medicine, Dankook University, Cheonan, Republic of Korea. , (North Korea)
Type
Published Article
Journal
Head & neck
Publication Date
Nov 13, 2019
Identifiers
DOI: 10.1002/hed.25980
PMID: 31721360
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The aim of study is to investigate the role of transient receptor potential cation channel subfamily V member 1 (TRPV1) on xerostomia-induced inflammatory response in vivo. Parotid, submandibular, and lingual gland were removed for xerostomia induction. The expression of inflammatory cytokines, TRPV1, NFkB, and MAPK in xerostomia was evaluated and compared in both TRPV1 wild and knockout mice. The level of interleukin-6 (IL-6) and IL-17, neutrophil/CD4 T-cell infiltration, phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N terminal kinase, TRPV1, and the localization of NFkB were elevated in xerostomia-induced TRPV1 wild-type mice. In contrast, inflammatory cytokines and MAPK were decreased in xerostomia-induced TRPV1 knockout mice. TRPV1 antagonist treatment also reduced tongue ulceration, neutrophil/CD4+ T-cell expression, IL-6, and IL-17 in TRPV1 wild-type mice. TRPV1 had a crucial role in modulating inflammation in xerostomia and targeting TRPV1 might be a promising therapeutic strategy for xerostomia. © 2019 Wiley Periodicals, Inc.

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