Abstract

Gintonin-enriched fraction (GEF), a bioactive glycolipoprotein derived from Panax ginseng is known for its potential as a natural anti-inflammatory agent. Keratinocytes are closely related to the development and progression of various inflammatory skin conditions. However, the effect of GEF on inflammation-related responses in keratinocytes remains unclear. This study aimed to investigate whether GEF modulates key inflammatory responses in keratinocytes stimulated by tumor necrosis factor (TNF)-α. The effect of GEF on biological activities in TNF-α-stimulated keratinocytes (HaCaT cells) was evaluated using water-soluble tetrazolium salt, enzyme-linked immunosorbent, immunostaining, and immunoblotting assays. In TNF-α-stimulated HaCaT cells, GEF attenuated reactive oxygen species production, nitric oxide release, and inducible nitric oxide synthase expression. Moreover, GEF reduced the release of interleukin (IL)-6 and RANTES, while increasing the release of IL-10 in TNF-α-exposed HaCaT cells. Additionally, GEF treatment resulted in reduced cyclooxygenase-2 expression and prostaglandin E2 release and inhibited TNF-α-induced translocation of nuclear factor-κB in HaCaT cells. Furthermore, TNF-α and IL-6 levels in ultraviolet B-irradiated HaCaT cells were reduced by GEF treatment. These findings indicated that GEF exerts anti-inflammatory effects on keratinocytes. This study provides a basis for the development of novel therapeutic approaches for the prevention and treatment of inflammatory skin disorders.

Affiliated Institutions

Related Publications

Publication Info

Year
2025
Type
article
Volume
26
Issue
24
Pages
11864-11864
Citations
0
Access
Closed

External Links

Social Impact

Social media, news, blog, policy document mentions

Citation Metrics

0
OpenAlex

Cite This

Rami Lee, Kyung‐Jong Won, Ji-Hun Kim et al. (2025). Potential Anti-Inflammatory Effects of Gintonin-Enriched Fraction in TNF-α-Stimulated Keratinocytes. International Journal of Molecular Sciences , 26 (24) , 11864-11864. https://doi.org/10.3390/ijms262411864

Identifiers

DOI
10.3390/ijms262411864