Treatment with Peanut Sprout Root Extract Alleviates Inflammation in a Lipopolysaccharide-Stimulated Mouse Macrophage Cell Line by Inhibiting the MAPK Signaling Pathway.

Yun Mi Lee,Eunjung Son,Dong-Seon Kim

doi:10.3390/ijms20235907

Abstract

Inflammation is a key response of the immune system to infection but aberrant inflammatory activity can lead to tissue damage and inflammatory diseases. Increasing evidence suggests that peanut sprout root extract (PSRE) has anti-inflammatory activity, and the aim of this study is therefore to investigate the effects of PSRE on the inflammatory response and the molecular mechanisms underpinning this effect in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Using a combination of cell viability, ELISA, and nitric oxide (NO) assays, together with Western blotting, we showed that PSRE effectively inhibited NO production in LPS-stimulated cells and significantly reduced the expression of pro-inflammatory cytokines, including IL-6, IL-1β, and PGE2, at a dose of 200 µg/mL of PSRE, whereas TNF-α expression tended to decrease under PSRE treatment. We also confirmed a dose-dependent and significant inhibition of iNOS and COX-2 protein expression. In addition, PSRE treatment induced anti-inflammatory effects by inhibiting the phosphorylation of MAPKs (ERK, JNK, and p38) and NF-κB activation. Our results indicate that the anti-inflammatory properties of PSRE may result from inhibition of the MAPK pathways, which are known promoters of cytokine secretion.

Highlights

Inflammation is a local response of the immune system to pathogens and damaged cells and is a vital defense mechanism [1]
peanut sprouts (PS) extracts extracts have have analyzed analyzed their their chemical chemical composition composition and and Several described a wide range of compounds, the levels of which vary over the course of germination
peanut sprout root extract (PSRE) treatment blocks was remarkably attenuated by. These results suggest that the p38 mitogen-activated protein kinase (MAPK), ERK, and JNK pathways to exert its anti-inflammatory effects on LPS-treated RAW

Summary

Introduction

Inflammation is a local response of the immune system to pathogens and damaged cells and is a vital defense mechanism [1]. Macrophages play an important role in the inflammatory response and are naturally activated by exposure to bacterial lipopolysaccharide (LPS), which increases their capacity for phagocytosis during the removal of infectious agents. Activated macrophages overexpress several mediators of inflammation in response to LPS-induced cell injury, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), prostaglandin E2 (PGE2), nitric oxide (NO), inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2 [3,4,5]. Members of the mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways have been shown to control the mechanisms of the inflammatory response in LPS-stimulated macrophages. The anti-inflammatory effects of suppressing cytokine production by inhibiting MAPK signaling and NF-κB transactivation have been considered targets for therapies aimed at reducing LPS-induced inflammation, and the levels of these cytokines have been frequently used as markers to assess the activity of anti-inflammatory drugs

Objectives

Methods

Results

Discussion

Conclusion