Toluhydroquinone inhibits inflammatory mediators through NF-κB and MAPKs pathways in LPS-induced RAW264.7 cells

Abstract

Chemotherapeutic agents from several metabolites are used to treat many diseases. There are diverse marine organisms such as invertebrates, algae, bacteria, and fungi, which produce secondary metabolites. Toluhydroquinone is a secondary metabolites product of marine fungi Phoma herbarum and its bioactivity is rarely known. The purpose of this study is to investigate the anti-inflammatory mechanism of toluhydroquinone in lipopolysaccharide (LPS) -induced RAW264.7 cells. Toluhydroquinone inhibited nitric oxide (NO) production and prostaglandin E2 (PGE2), as well as reduced inflammatory mediator proteins including inducible nitric oxide synthase (iNOS) and cyclooxyganse-2 (COX-2) expression. Toluhydroquinone decreased the pro-inflammatory cytokines expression of tumor necrosis factor-α (TNF-α), interleukine-1β (IL-1β), and interleukin-6 (IL-6). Additionally, toluhydroquinone inhibited the phosphorylation of nuclear factor-κB (NF-κB). Also, toluhydroquinone reduced the phosphorylation of mitogen-activated protein kinases (MAPKs) pathway, which is involved extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and p38. Moreover, toluhydroquinone induced heme oxygenase-1 (HO-1) protein expression which is stress-inducible enzyme to effect cell protection, through nuclear factor E2-related factor 2 (Nrf2). These results indicate that the mechanism of toluhydroquinone effects on anti-inflammatory in LPS-stimulated RAW264.7 cells.