Curcumin Ameliorates Ovalbumin-Induced Atopic Dermatitis and Blocks the Progression of Atopic March in Mice

Inflammation. 2020 Feb;43(1):358-369. doi: 10.1007/s10753-019-01126-7.

Abstract

Curcumin, extracted from the roots of Curcuma longa, has been used as an anti-inflammatory agent since the time of Ayurveda. The present work was designed to evaluate the potential of curcumin in amelioration of ovalbumin (OVA) induced AD in mice. Female BALB/c mice were subjected to skin OVA-patch application for a period of 1 week followed by resting period of 2 weeks, and the same protocol was repeated thrice. Curcumin was administered daily at dose of 20 mg/kg (i.p.) for 7 consecutive days during last sensitization phase. The phytochemical ameliorated the OVA-induced skin pathology as evident by normalization of epidermal thickness and suppressed infiltration of inflammatory cells in dermal region. The expression of Th2 promoting cytokines (TSLP/IL-33) and Th2 cytokines (IL-4/IL-5/IL-13/IL-31) was suppressed markedly along with reduced STAT-6 phosphorylation and GATA-3 expression. Curcumin administration also restored the redox balance and phosphorylation status of P65-NF-κB. Additionally, the epicutaneously sensitized mice challenged with aerosolized OVA developed asthmatic features which were effectively thwarted back upon curcumin treatment as reflected by data on total/differential cells in BALF and mRNA expression of Th2 cytokines in lungs. Overall, our findings demonstrate that curcumin treatment blunts the development of AD as well as associated atopic march in experimental mice.

Keywords: asthma; atopic dermatitis; atopic march; curcumin; ovalbumin.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Asthma / chemically induced
  • Asthma / immunology
  • Asthma / metabolism
  • Asthma / prevention & control
  • Curcumin / pharmacology*
  • Cytokines / metabolism
  • Dermatitis, Atopic / chemically induced
  • Dermatitis, Atopic / immunology
  • Dermatitis, Atopic / metabolism
  • Dermatitis, Atopic / prevention & control*
  • Disease Models, Animal
  • Disease Progression
  • Female
  • GATA3 Transcription Factor / metabolism
  • Lung / drug effects
  • Lung / immunology
  • Lung / metabolism
  • Mice, Inbred BALB C
  • Ovalbumin
  • Phosphorylation
  • STAT6 Transcription Factor / metabolism
  • Skin / drug effects*
  • Skin / immunology
  • Skin / metabolism
  • Skin / pathology
  • Th2 Cells / drug effects
  • Th2 Cells / immunology
  • Th2 Cells / metabolism
  • Transcription Factor RelA / metabolism

Substances

  • Anti-Inflammatory Agents
  • Cytokines
  • GATA3 Transcription Factor
  • Gata3 protein, mouse
  • Rela protein, mouse
  • STAT6 Transcription Factor
  • Stat6 protein, mouse
  • Transcription Factor RelA
  • Ovalbumin
  • Curcumin