Chitosan oligosaccharide-mediated attenuation of LPS-induced inflammation in IPEC-J2 cells is related to the TLR4/NF-κB signaling pathway
Chitosan oligosaccharide-mediated attenuation of LPS-induced inflammation in IPEC-J2 cells is related to the TLR4/NF-κB signaling pathway
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DOI：
10.1016/j.carbpol.2019.05.036
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发表时间：
2019-09-01
影响因子：
11.2
通讯作者：
Ju, Xianghong
中科院分区：
文献类型：
--
作者：
Shi, Lin;Fang, Biao;Ju, Xianghong
本文报道了壳寡糖（COS）对脂多糖（LPS）诱导的IPEC-J2和DSS葡聚糖硫酸钠（DSS）诱导的结肠炎小鼠炎症反应的保护机制。暴露于LPS后，IPEC-J2细胞的增殖率显著降低，上皮细胞的完整性受到损害。然而，COS预处理显着降低这些变化。低浓度（200 μ g/mL）COS上调Toll样受体4（TLR 4）和核p65的表达，但抑制LPS诱导的核p65，IL-6和IL-8的表达。TLR 4抑制剂的加入降低了单独暴露于COS或LPS的IPEC-J2细胞中的核p65、IL-6和IL-8表达，并且在COS和LPS共处理的细胞中观察到核p65的轻微上调。中剂量COS（600 mg/kg/d）对DSS诱导的结肠炎具有保护作用，其中TLR 4和核p65表达水平降低。我们推测COS对IPEC-J2细胞和小鼠中LPS和DSS诱导的炎症反应的预防与TLR 4/NF-κ B信号通路的抑制有关。
The protective mechanism of chitosan oligosaccharide (COS) against lipopolysaccharides (LPS) -induced inflammatory responses in IPEC-J2 and in mice with DSS dextran sulfate sodium (DSS) -induced colitis is reported. Upon exposure to LPS, the proliferation rate of IPEC-J2 cells markedly decreased, and epithelial cell integrity was compromised. However, COS pretreatment significantly reduced these changes. Low-concentration (200 mu g/mL) COS up-regulated Toll-like receptor 4 (TLR4) and nuclear p65 expression, but inhibited LPS-induced expression of nuclear p65, IL-6, and IL-8. Addition of the TLR4 inhibitor reduced nuclear p65, IL-6, and IL-8 expression in IPEC-J2 cells exposed to COS or LPS alone, and a slight up-regulation in nuclear p65 was observed in COS and LPS co-treated cells. Medium-dose COS (600 mg/kg/d) protected against DSS-induced colitis, in which TLR4 and nuclear p65 expression levels were decreased. We postulate that the prevention of both LPS- and DSS -induced inflammatory responses in IPEC-J2 cells and mice by COS are related to the inhibition of the TLR4/NF-kappa B signaling pathway.