Dithranol abolishes UCH-L1 immunoreactivity in the nerve fibers of the rat orofacial skin

Ivan Orojan, Csaba Szigeti, Szilvia Varszegi, Endre Dobo, Karoly Gulya

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Dithranol has been used to treat psoriasis for decades. Although its beneficial effect may involve the induction of cutaneous inflammation, and inflammation often leads to damages in nerve fibers, these alterations are not well documented. Therefore, we investigated the effects of dithranol on the immunohistochemical characteristics of the cutaneous nerve fibers in the rat skin. Epidermal nerve fiber staining was achieved with ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) immunohistochemistry in the orofacial skin of control rats, rats treated with (a) dithranol for 5 days, (b) corticosteroid for 5 days following dithranol treatment for 5 days, and (c) corticosteroid for 5 days. The results revealed a complete loss of UCH-L1 immunoreactivity in the dithranol-treated animals. Topical application of corticosteroid onto the inflamed skin for 5 days reversed this effect: the UCH-L1 immunoreactivity was almost completely restored. Steroid treatment for 5 days did not change the appearance of the UCH-L1-immunoreactive nerve fibers. These findings were supported by Western blot analyses. We conclude that dithranol, incidentally similarly to psoriasis, causes inflammation and abolishes UCH-L1 immunoreactivity in the rat orofacial skin in a corticosteroid-reversible manner. This phenomenon may be due to the ability of dithranol to cause oxidative damage to the UCH-L1 protein, and to the antioxidant activity of the corticosteroids countering this effect.

Original languageEnglish
Pages (from-to)216-220
Number of pages5
JournalBrain research
Volume1121
Issue number1
DOIs
Publication statusPublished - Nov 22 2006

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Keywords

  • Dithranol
  • Inflammation
  • Nerve fiber
  • Protein gene product 9.5
  • Rat
  • Skin
  • Ubiquitin carboxyl-terminal hydrolase L1

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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