# Oxytropis falcata bunge extract combined with black soybean oil ameliorates DNCB-induced atopic dermatitis-like skin inflammation

## TL;DR

A combination of Oxytropis falcata extract and black soybean oil reduces atopic dermatitis symptoms in mice without causing skin toxicity.

## Contribution

The study demonstrates the efficacy of combining traditional and modern treatments for atopic dermatitis in a preclinical model.

## Key findings

- The combination of OFE and BSO showed the most significant improvement in epidermal thickness and dermatitis severity.
- The treatment suppressed the HDAC3/NF-κB signaling pathway, a key driver of inflammation.
- No skin toxicity was observed, suggesting a safe therapeutic approach.

## Abstract

Oxytropis falcata Bunge (OF) is a traditional Tibetan medicine, while black soybean oil (BSO) is a contemporary treatment used for eczema. Pharmacological studies have indicated that both exhibit strong anti-inflammatory effects. However, the role of OF in atopic dermatitis remains uncertain.

To investigate the anti-inflammatory effects and underlying mechanisms of O. falcata Bunge extracts (OFE) and BSO in DNCB-induced atopic dermatitis in mice.

Mice were divided into six groups: positive control (1% mometasone furoate), OFE, BSO, OFE + BSO, DNCB, and control. After 20 days of local application of each ointment, therapeutic effects were evaluated. Histopathological examination was performed to assess skin thickness and mast cell infiltration. ELISA was used to quantify proinflammatory cytokines, real-time PCR measured IL-36 mRNA levels, and Western blotting analyzed HDAC3/NF-κB and CysLTR1 protein expression.

All treatments alleviated DNCB-induced atopic dermatitis symptoms, with the combination group showing the most significant improvement in epidermal thickness, mast cell infiltration, and dermatitis severity. In addition, the treatment groups suppressed activation of the HDAC3/NF-κB signaling pathway.

The combination of OFE and BSO can effectively reduce DNCB-induced atopic dermatitis in mice. Its action does not rely on broad immunosuppression or induce skin toxicity and may involve inhibition of proinflammatory cytokine release and downregulation of the HDAC3/NF-κB signaling pathway.