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TRPV1 is known to mediate itch and neurogenic inflammation, but the role of TRPV1 in itch\u2010associated scratching in AD is poorly understood. In this study, we examined the efficacy of cutting off nails\u00a0and TRPV1 antagonist, ruthenium red (RR) in a murine model of AD induced by DNFB and further investigated the underlying mechanism. Nail clipping or RR could markedly ameliorate the general AD\u2010like symptoms as manifested by the reduced clinical severity of dermatitis, IgE and Th2\u2010related cytokine levels, and mast cell degranulation. Moreover, scratching behaviour, the levels of pruritogenic mediators, including HIS, TSLP, IL\u201031 and SP, and skin pH and TEWL were all significantly decreased in nail clipping or RR\u2010treated mice, suggesting a reduction in itch\u2010associated scratching and skin barrier defects. Immunofluorescence staining and Western blot results revealed that\u00a0antipruritic\u00a0effect of\u00a0nail clipping or RR in AD may be explained, at least in part, by the suppression of TRPV1 activation. In summary, these data show that TRPV1\u00a0mediates itch\u2010associated scratching and subsequent skin barrier defects, suggesting its potential as a therapeutic target in AD.<\/jats:p>","DOI":"10.1111\/exd.14464","type":"journal-article","created":{"date-parts":[[2021,10,6]],"date-time":"2021-10-06T08:49:52Z","timestamp":1633510192000},"page":"398-405","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["TRPV1 mediates itch\u2010associated scratching and skin barrier dysfunction in DNFB\u2010induced atopic dermatitis mice"],"prefix":"10.1111","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1599-7061","authenticated-orcid":false,"given":"Liu","family":"Tang","sequence":"first","affiliation":[{"name":"Department of Pharmacy Renmin Hospital of Wuhan University Wuhan China"},{"name":"School of Pharmaceutical Sciences Wuhan University Wuhan 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