Pegia sarmentosa extract modulates psoriatic inflammation through chemokine and antimicrobial peptide (AMP) inhibition in HaCaT keratinocyte

Psoriasis is a refractory autoimmune skin disease characterized by epidermal proliferation and excessive inflammatory responses.Approximately 10 medicinal plants used to treat skin diseases were selected from the resource database of the Korea Research Institute of Bioscience and Biotechnology (KRIBB) International Biomaterials Research Center.Pegia sarmentosa is known for its antipyretic, analgesic, and blood circulation-enhancing effects.In this study, we examined the anti-inflammatory effects of Pegia sarmentosa extract (PSE) using a human keratinocytebased psoriasis cell model.The total polyphenol content of PSE was analyzed to be approximately 224.22±3.45mg GAE/g, and its free radical scavenging activity was confirmed using the DPPH/ ABTS assay.Furthermore, in a CCK-8 assay using HaCaT cells, no cytotoxicity was observed up to 10 μg/mL, approximately 92% was observed at 30 μg/mL, and approximately 50% was observed at 50 μg/mL.Therefore, to exclude the possibility of transcriptional inhibition due to cytotoxicity, the maximum concentration was set at 10 μg/mL and applied to all cell experiments.In HaCaT cells stimulated with TNF-α/IL-17A/IFN-γ (20 ng/mL), PSE dose-dependently downregulated the mRNA expression of major inflammatory markers, including IL-1α, IL-1β, IL-36γ, and MIR146A.In addition, PSE significantly suppressed the expression of antimicrobial peptides (LL-37, β-defensin 2, S100A7/A8) and major psoriasis-related chemokines (CXCL8, CCL20).Furthermore, Western blot analysis showed that PSE significantly inhibited the phosphorylation of NF-kB/AKT proteins.This suggests that PSE may help alleviate excessive inflammation, a hallmark of psoriasis, by suppressing psoriatic inflammatory signaling through inhibition of the NF-kB and AKT pathways in TNF-α/IL-17A/IFN-γstimulated HaCaT cells.