Related Experiment Video
Updated: Jul 3, 2026

A Mouse Ear Model for Allergic Contact Dermatitis Evaluation
Published on: March 24, 2023
Indole-3-carbinol attenuates DNCB-induced atopic dermatitis in mice by reducing inflammation and IL-4/IL-13
Rabbia Kalim1, Arham Shabbir1, Hafsa Nasr1
1Department of Pharmacology, Institute of Pharmacy, Faculty of Pharmaceutical and Allied Health Sciences, Lahore College for Women University, Lahore, Pakistan.
Abstract:
Atopic dermatitis (AD), commonly known as atopic eczema, is a chronic inflammatory skin disease. Indole-3-carbinol (I3C), a phytochemical naturally occurring in Brassica vegetables, has been traditionally used in folk medicine for inflammatory and metabolic disorders. This study investigated the immunomodulatory and anti-inflammatory effects of I3C in a mouse model of 1-chloro-2,4-dinitrobenzene (DNCB)-induced atopic dermatitis. Atopic dermatitis was induced by DNCB sensitization on days 0 and 3. Following disease confirmation on day 7, mice received daily oral or topical administrations of I3C or prednisolone from day 7 to day 19. Macroscopic evaluations included dorsal skin and ear thickness measurements. Histopathological changes were assessed using hematoxylin and eosin staining, and hematological parameters were also analyzed. Gene expression of interleukin (IL)-4 and IL-13 in ear tissue was quantified by real-time polymerase chain reaction (RT-qPCR). Computational molecular docking was performed to determine I3C's affinity for both cytokines. The data indicated that I3C attenuated DNCB-induced AD-like symptoms following both oral and topical administration. Treatment with I3C also resulted in reduced ear thickness. Hematological analysis revealed significantly decreased total leukocyte counts (TLC) and a general downward numerical trend in differential leukocyte count (DLC) parameters in I3C-treated groups. Histopathological evaluation confirmed that I3C ameliorated skin thickening and reduced inflammatory cell infiltration. Furthermore, IL-4 and IL-13 expression levels were decreased in I3C-treated groups. Molecular docking analysis demonstrated moderate binding affinities of -5.1 kcal/mol and -5.3 kcal/mol with IL-4 and IL-13, respectively. In conclusion, findings from this exploratory study suggest that I3C treatment ameliorated DNCB-induced atopic dermatitis in mice, evidenced by reductions in ear thickness and IL-4/IL-13 mRNA expression. Molecular docking analysis demonstrated moderate binding affinities of I3C toward IL-4 and IL-13, providing supportive evidence of potential ligand-protein interactions.

