AI Article Synopsis
- The study aimed to explore how chitosan oligosaccharides (COS) can inhibit IL-8 production in human umbilical vein endothelial cells (HUVECs) triggered by lipopolysaccharides (LPS).
- Various techniques, including RT-PCR, ELISA, and Western blotting, were employed to analyze IL-8 expression and the associated signaling pathways, while additional assays assessed HUVEC migration and adhesion of monocyte cells.
- Results showed that COS significantly reduced LPS-induced IL-8 levels and hindered HUVEC migration and monocyte adhesion in a dose-dependent manner, likely by blocking key signaling pathways like p38 MAPK and PI3K/Akt.
Article Abstract
Aim: To investigate whether and how COS inhibited IL-8 production in LPS-induced human umbilical vein endothelial cells (HUVECs).
Methods: RT-PCR, enzyme-linked immunosorbent assays (ELISA) and Western blotting were used to study IL-8 expression and related signaling pathway. Wound healing migration assays and monocytic cell adhesion analysis were used to explore the chemotactic and adhesive activities of HUVECs.
Results: COS 50-200 μg/mL exerted a significant inhibitory effect on LPS 100 ng/mL-induced IL-8 expression in HUVECs at both the transcriptional and translational levels. In addition, COS 50-200 μg/mL inhibited LPS-induced HUVEC migration and U937 monocyte adhesion to HUVECs in a concentration-dependent manner. Signal transduction studies suggest that COS blocked LPS-induced activation of nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) as well as phosphorylation of p38 mitogen-activated protein kinase (MAPK) and phosphokinase Akt. Further, the over-expression of LPS-induced IL-8 mRNA in HUVECs was suppressed by a p38 MAPK inhibitor (SB203580, 25 μmol/L) or a phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002, 50 μmol/L).
Conclusion: COS inhibited LPS-induced IL-8 expression in HUVECs through the blockade of the p38 MAPK and PI3K/Akt signaling pathways.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4001981 | PMC |
| http://dx.doi.org/10.1038/aps.2011.10 | DOI Listing |
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