Spartina anglica extract attenuates TNF-α/IFN-γ-induced inflammatory responses in HaCaT keratinocytes through suppression of the MAPK, NF-κB, and STAT1 signaling pathways

This study investigated the anti-inflammatory effects of Spartina anglica extract (SAE) in a human keratinocyte model of inflammation. HaCaT cells were stimulated with tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) to induce inflammatory responses. Cell viability was assessed using the MTT assay to determine non-cytotoxic concentrations. The expression of the chemokines TARC/CCL17 and macrophage-derived chemokine MDC/CCL22 was quantified at both the mRNA and protein levels using quantitative real-time PCR and ELISA, respectively. In addition, the activation of key inflammatory signaling pathways was evaluated by Western blot analysis. SAE did not exhibit cytotoxic effects at concentrations up to 250 μg/mL. Under inflammatory conditions, SAE significantly reduced the expression of CCL17 and CCL22 in a dose-dependent manner. Mechanistically, this suppression was associated with decreased phosphorylation of MAPK signaling components, including ERK, JNK, and p38, as well as inhibition of NF-κB and STAT1 activation. High-performance liquid chromatography analysis revealed a major peak corresponding to the retention time of iso-orientin in SAE. These findings suggest that SAE may attenuate keratinocyte-mediated inflammatory responses through modulation of chemokine expression and key intracellular signaling pathways.