Anti-Inflammatory Activity of Dichondra micrantha Extract and Its Potential as a Functional Cosmetic Ingredient

This study aimed to evaluate the anti-inflammatory activity of Dichondra micrantha ethanol extract (DM-EE) and to elucidate its regulatory effects on the NF-κB and AP-1 signaling pathways in vitro. Ethanolic extract of Dichondra micrantha was prepared and tested in RAW264.7 macrophages. Cell viability was assessed using the MTT assay, and nitric oxide (NO) production was measured in cells stimulated with lipopolysaccharide (LPS), polyinosinic–polycytidylic acid [Poly I:C], and Pam3CSK4. In addition, AP-1 and NF-κB luciferase reporter assays, RT-PCR analysis of inflammatory mediators, and Western blot analysis of phosphorylated signaling proteins were performed. DM-EE exhibited no significant cytotoxicity within the tested concentration range. It significantly inhibited LPS-, Poly I:C-, and Pam3CSK4-induced NO production in a concentration-dependent manner, with the strongest inhibitory effect observed at 200 μg/mL. Moreover, DM-EE suppressed LPS- and Poly I:C-induced AP-1 and NF-κB transcriptional activity. RT-PCR analysis revealed that DM-EE downregulated the mRNA expression of inflammatory mediators, including iNOS, COX-2, and IL-1β, in LPS-stimulated RAW264.7 cells. Consistently, Western blot analysis showed that DM-EE reduced the phosphorylation levels of p65 and c-Jun, indicating inhibition of NF-κB and AP-1 activation. These findings demonstrate that DM-EE exerts significant anti-inflammatory effects by attenuating macrophage-mediated inflammatory responses through suppression of the NF-κB and AP-1 signaling pathways. Therefore, Dichondra micrantha extract showed potential as a natural bioactive material with anti-inflammatory properties under in vitro conditions.