Abstract
In our previous work, Asterina pectinifera was fermented with Cordyceps militaris mycelia to improve its bioactivities and was reported to have strong antioxidant activities. The aim of the current study was to investigate its anti-inflammatory effect and mechanisms of action. In this study, we observed the inhibitory effect of the extract from fermented A. pectinifera with C. militaris mycelia (FACM) on nitric oxide (NO) production and its molecular mechanism in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. FACM could decrease LPS-induced NO production. Western blot analysis showed that FACM could down-regulate LPS-induced expression of inducible NO synthase without affecting cyclooxygenase-2. Moreover, FACM exhibited anti-inflammatory activity in LPS-induced RAW264.7 mouse macrophage cells through proinflammatory mediators including TNF-α and IL-6 via nuclear factor kappa B pathway. FACM inhibited LPS-induced phosphorylation of extracellular-signal-regulated kinase expression. Our results suggest that FACM may be a potential candidate for inflammation therapy by attenuating the generation of cytokines, production of NO, and generation of ROS in RAW264.7 cells.