Sargachromenol Attenuates Inflammatory Responses by Regulating NF- B and Nrf2 Pathways in RAW 264.7 Cells and LPS-treated Mice

This study aims to explore the anti-inflammatory mechanisms of sargachromenol in both RAW 264.7 cells and lipopolysaccharide (LPS)-treated mice, as previous reports have suggested that sargachromenol possesses anti-aging, anti-inflammatory, antioxidant, and neuroprotective properties. Although the precise mechanism behind its anti-inflammatory activity remains unclear, pretreatment with sargachromenol effectively reduced the production of nitric oxide, prostaglandin E 2 , and interleukin (IL)-1 beta in LPS-stimulated RAW 264.7 cells by inhibiting cyclooxygenase-2. Moreover, sargachromenol inhibited the activation of nuclear factor- kappa B (NF- kappa B) by preventing the degradation of the inhibitor of kappa B- alpha (I kappa B- alpha ) and inhibiting protein kinase B (Akt) phosphorylation in LPS-stimulated cells. We also found that sargachromenol induced the production of heme oxygenase-1 (HO-1) by activating the nuclear transcription factor erythroid-2-related factor 2 (Nrf2). In LPS-treated mice, oral administration of sargachromenol effectively reduced the levels of IL-1 beta , IL-6, and tumor necrosis factor- alpha (TNF- alpha ) in the serum, suggesting its ability to suppress the production of inflammatory mediators by inhibiting the Akt/NF- kappa B pathway and upregulating the Nrf2/HO-1 pathway.