J Bacteriol Virol.  2016 Dec;46(4):288-294. 10.4167/jbv.2016.46.4.288.

Acrosorium polyneurum Extract Inhibits the LPS-Induced Inflammatory Response by Impairing the MAPK and NF-κB Pathways

Affiliations
  • 1Department of Microbiology and Immunology, School of Medicine and Brain Korea 21 PLUS Program, Jeju National University, Jeju, Korea. yskoh7@jejunu.ac.kr
  • 2Institute of Medical Science, Jeju National University, Jeju, Korea.

Abstract

Marine algae exhibit broad spectrum anti-bacterial and anti-inflammatory activities. Acrosorium polyneurum (A. polyneurum) is a marine red alga and belongs to the family Delesseriaceae. The present research evaluates the antiinflammatory effects of A. polyneurum extract (APE) on pro-inflammatory cytokine production. APE demonstrated substantial inhibitory effects on production of pro-inflammatory cytokine in bone marrow-derived macrophages (BMDMs). APE pre-treatment in the lipopolysaccharide (LPS)-stimulated BMDMs exhibited a robust inhibitory effect on production of interleukin (IL)-12, IL-6 and tumor necrosis factor (TNF)-α. It revealed a robust inhibitory effect on phosphorylation of ERK1/2, JNK1/2 and p38. APE also showed remarkable inhibitory effect on phosphorylation and degradation of IκBα. Furthermore, APE pre-treatment demonstrated substantial inhibition of LPS-induced production of nitric oxide and inducible nitric oxide synthase. Collectively, these data suggest that APE has a noteworthy anti-inflammatory property and deserve further studies concerning its potential use as a medicinal agent for inflammation-related disorders.

Keyword

Acrosorium polyneurum; Mitogen-activated protein kinase; NF-κB; Nitric oxide; Pro-inflammatory cytokine

MeSH Terms

Hominidae
Humans
Interleukin-6
Interleukins
Macrophages
Nitric Oxide
Nitric Oxide Synthase Type II
Phosphorylation
Tumor Necrosis Factor-alpha
Interleukin-6
Interleukins
Nitric Oxide
Nitric Oxide Synthase Type II
Tumor Necrosis Factor-alpha

Figure

  • Figure 1. Inhibitory effects of Acrosorium polyneurum Extract (APE) on cytokine production in LPS-stimulated BMDMs. (A-C) Before stimulation with LPS (10 ng ml-1), BMDMs were treated with APE at various doses as shown for 1 h and cytokines levels were assessed by ELISA. ND, not detectable; APE, A. polyneurum extract. ∗p < 0.05, ∗∗p < 0.01 vs. APE-untreated cells in the presence of LPS.

  • Figure 2. Inhibitory effects of APE on phosphorylation of MAPKs by LPS-stimulated BMDMs. (A) Cells were pre-treated with or without APE (25 μg ml-1) for 1 h before stimulation with LPS (10 ng ml-1). Total cell lysate was obtained at various time intervals as shown. Western blot analysis was done on the cell lysate to evaluate phosphorylation of ERK1/2, JNK1/2 and p38. Total ERK1/2 MAPK was taken as the loading control. (B) Phosphorylation of MAPKs protein was quantified using scanning densitometry. ∗p < 0.05 vs. APE-untreated cells in the presence of LPS.

  • Figure 3. Inhibitory effects of APE on NF-κB activation by LPS- stimulated BMDMs. (A) Cells were treated as described in Fig. 2A, and Western blot analysis was performed. (B) Scanning densitometry was performed as described in Fig. 2B. ∗ p < 0.05 vs. APE-untreated cells in the presence of LPS.

  • Figure 4. Inhibitory effects of APE on the production of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) in LPS-stimulated RAW264.7 cells. RAW264.7 cells were pre-treated or not treated with APE at various doses as shown for 1 h before stimulation with LPS (10 ng ml-1). (A) The NO production was investigated by Griess assay. (B) The protein levels of iNOS were measured by Western blot analysis and β-actin was used as the loading control. (C) For quantification of iNOS protein expression scanning densitometry was used and normalized by that of β-actin. ∗ p < 0.05, ∗∗ p < 0.01 vs. APE-untreated cells in the presence of LPS.


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