Abstract
Fermented and aged mountain-cultivated ginseng sprouts (FAMCGS) exhibit superior antioxidant and anti-inflammatory properties compared to mountain-cultivated ginseng sprouts (MCGS). However, the mechanisms behind these properties of FAMCGSE remain unclear. This study explores the anti-inflammatory effects of FAMCGS extract (FAMCGSE) on LPS-stimulated RAW 264.7 macrophages and the underlying mechanisms. The MTT assay confirmed that FAMCGSE (0 to 0.1%) maintained cell viability without inducing morphological changes. Pretreatment with FAMCGSE significantly mitigated LPS-induced morphological alterations dose-dependently. RT-PCR and Western blot analyses showed that FAMCGSE significantly reduced the mRNA and protein levels of proinflammatory mediators such as TNF-α, IL-1β, IL-6, iNOS, and COX-2. Additionally, FAMCGSE decreased the production of TNF-α, IL-1β, IL-6, nitric oxide, and PGE2 in LPS-activated RAW264.7 cells. Mechanistically, FAMCGSE inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs; ERK, p38, and JNK) and prevented the LPS-induced nuclear translocation of NF-κB, with effects comparable to compound K (CK) or dexamethasone. Notably, FAMCGSE was particularly effective in inhibiting ERK and JNK activation, with less impact on p38, suggesting a specific inhibitory action on certain MAPK pathways. These findings highlight FAMCGSE's potential as an inhibitor of MAPK and NF-κB pathways, indicating that FAMCGSE, including its main component CK, may be a promising therapeutic agent for inflammation-related conditions.