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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 anti-inflammatory 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.
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 | 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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