ZHU Lingyu, ZHANG Ziqi, LAN Hainan, WU Min, LIU Huilin, ZHENG Xin. Effects of astaxanthin on IPEC-J2 cell inflammation induced by lipopolysaccharide via TLR4/MyD88/NF-κB signaling pathway[J]. Journal of South China Agricultural University, 2018, 39(5): 53-58. DOI: 10.7671/j.issn.1001-411X.2018.05.008
    Citation: ZHU Lingyu, ZHANG Ziqi, LAN Hainan, WU Min, LIU Huilin, ZHENG Xin. Effects of astaxanthin on IPEC-J2 cell inflammation induced by lipopolysaccharide via TLR4/MyD88/NF-κB signaling pathway[J]. Journal of South China Agricultural University, 2018, 39(5): 53-58. DOI: 10.7671/j.issn.1001-411X.2018.05.008

    Effects of astaxanthin on IPEC-J2 cell inflammation induced by lipopolysaccharide via TLR4/MyD88/NF-κB signaling pathway

    • Objective  To investigate the effect of astaxanthin (AST) on IPEC-J2 cell inflammation induced by lipopolysaccharide (LPS) via TLR4/MyD88/NF-κB signaling pathway.
      Method  MTT assay was performed to determine the optimal time and concentrations of astaxanthin and LPS for treating IPEC-J2 cells and transfected IPEC-J2 cells. Fluorescent quantitative RT-PCR was performed to determine the relative mRNA expressions of inflammatory factors including NF-κB, TNF-α, IL-6 and IL-1β in IPEC-J2 cells and transfected IPEC-J2 cells stimulated by LPS. ELISA assays were carried out to determine the secretion amounts of these inflammatory factors.
      Result  The vitality of IPEC-J2 cells and transfected IPEC-J2 cells reached the peak when treated with 150 μmol·L–1 astaxanthin for 3 h or 100 ng·mL–1 lipopolysaccharide for 6 h. Compared with control group, the relative mRNA expressions and secretions of NF-κB, TNF-α, IL-6 and IL-1β in IPEC-J2 cells significantly increased in LPS treatment group (P<0.05). Compared with LPS treatment group, the relative mRNA expressions and secretions of NF-κB, TNF-α, IL-6 and IL-1β in LPS+AST group were significantly lower in IPEC-J2 cells (P<0.05), but did not differ significantly in transfected IPEC-J2 cells (P>0.05).
      Conclusion  Astaxanthin can inhibit cell inflammation, and its protective effect on cells is related to TLR4/MyD88/NF-κB signaling pathway.
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