Polyphenols Extracted from Hizikia fusiformis Relieves Lipopolysaccharide-Induced Inflammation in RAW264.7 Cells via the Nuclear Factor-κB/Mitogen-Activated Protein Kinase Signaling Pathways

To study the effect of Hizikia fusiformis polyphenols (HFPs) on lipopolysaccharide (LPS)-induced inflammatory response in RAW264.7 cells.

The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method was used to examine the cellular viability. Nitric oxide (NO) was measured by the Griess method. Quantitative real-time polymerase chain reaction (qPCR) was applied to analyze the gene expression of interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). Flow cytometry was used to determine macrophage phagocytosis. The expression of the key proteins involved in the mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB signaling pathways was investigated by Western blot.

HFPs at concentrations of 0–160 μg/mL had no cytotoxic effect on RAW264.7 cells. Compared with the LPS-induced group, HFPs dose-dependently inhibited the phagocytic capacity of macrophage and NO production. Besides, the mRNA levels of several inflammatory mediators, including IL-1β, IL-6, TNF-α, iNOS and COX-2 were down-regulated, and this effect was dependent on the dose of HFPs and LPCS stimulation time. The expression of these inflammatory mediators may be related to the inhibition of the activation of the activation of p38 MAPK and NF-κB p65 by HFPs.

HFPs alleviates LPS-induced inflammation in RAW264.7 cells by down-regulating the activation of the p38 MAPK and NF-κB p65 signaling pathways and inhibiting the transcription and expression of downstream inflammatory mediators.