# The stem of Schisandra chinensis and Schisandrin B alleviated DNCB-induced atopic dermatitis in mice by inhibiting the NF-κB pathway

## TL;DR

The stem of Schisandra chinensis and its compound Schisandrin B may help treat atopic dermatitis in mice by reducing inflammation and improving skin barrier function.

## Contribution

This study identifies Schisandra chinensis stem extract and Schisandrin B as novel therapeutic agents for atopic dermatitis via NF-κB pathway inhibition.

## Key findings

- Schisandra chinensis stem extract and Schisandrin B improved skin barrier function in AD mice.
- The compounds reduced inflammation and pruritus by suppressing IgE and mast cell mediators.
- NF-κB pathway modulation was identified as a potential mechanism of action.

## Abstract

Atopic dermatitis (AD) is a chronic, pruritic, inflammatory skin disorder. While the stem of Schisandra chinensis has been extensively studied for its pharmacological properties, including anti-inflammatory, antioxidant, and hepatoprotective effects, its therapeutic potential in AD remains to be elucidated. This study therefore aimed to investigate the effects of Schisandra chinensis stem extract (SCSE) against AD and to explore its underlying mechanism of action.

Chemical profiling of SCSE via UPLC-Q-Exactive-Orbitrap-MS revealed 45 constituents, with lignans comprising 80%. The primary active component was identified through activity-guided assays employing hyaluronidase inhibition and HPLC. The therapeutic efficacy of SCSE and its constituent Schisandrin B (Sch B) was assessed in an AD mouse model. Furthermore, network pharmacology predicted the involved signaling pathways, and these predictions were subsequently validated experimentally.

Sch B was identified as the core active component. Both SCSE and Sch B significantly improved skin barrier function in AD mice, as evidenced by reduced transepidermal water loss (TEWL) and upregulation of key barrier proteins (Filaggrin, Loricrin, and Claudin-1). They also alleviated pruritus by suppressing Transient Receptor Potential Vanilloid 1 (TRPV1) and mitigated the allergic-inflammatory response, as shown by reduced Immunoglobulin E (IgE) levels and inhibited release of mast cell (MC) mediators (IL-4, IL-6, TNF-α). These effects were potentially mediated through modulation of the NF-κB pathway.

By simultaneously mitigating skin barrier dysfunction, immune inflammation, and pruritus, SCSE and Sch B hold promise as therapeutic candidates capable of disrupting the self-perpetuating cycle of AD. These findings position SCSE and Sch B as a novel therapeutic strategy for this disease.