College of Animal Science and Technology, Northwest A&F University, Yangling, Xi'an, Shaanxi 712100, PR China; College of Basic Medical Science, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi 712000, PR China.
College of Animal Science and Technology, Northwest A&F University, Yangling, Xi'an, Shaanxi 712100, PR China.
Int J Biol Macromol. 2020 Sep 15;159:832-838. doi: 10.1016/j.ijbiomac.2020.05.005. Epub 2020 May 7.
As an immune-regulator, Astragalus polysaccharides (APS) could effectively modulate the activity of toll-like receptor 4 (TLR4) signaling pathway, and induce anti-inflammatory response in intestinal. Our research before indicated that toll/interleukin 1 receptor-domain-containing adapter-inducing interferon-b (TRIF) might be a critical regulator for APS. So, in this experiment, we analyzed the effects of APS on lipopolysaccharide (LPS)-infected Caco2 cells in the circumstances of TRIF knockout. By using qRT-PCR and flow cytometry method, we analyzed the genes expression at transcriptional and translational level, respectively. The results of genes expression at both transcription and translation level showed that LPS could activate the myeloid differentiation factor 88 (MyD88)-TNF receptor associated factor (TRAF) pathway downstream from TLR4, and induce the high expression of pro-inflammatory cytokines. However, APS could effectively suppress the LPS induced inflammatory response. While, in the context of TRIF knockout, APS couldn't effectively attenuate the LPS activated MyD88-TRAF6 pathway, as well as the expression of pro-inflammatory cytokines. Above all, we concluded that APS could antagonize the LPS induced inflammatory response by a TRIF-dependent manner.
作为一种免疫调节剂，黄芪多糖 (APS) 可以有效调节 Toll 样受体 4 (TLR4) 信号通路的活性，并在肠道中诱导抗炎反应。我们之前的研究表明，Toll/白细胞介素 1 受体结构域包含衔接诱导干扰素-β (TRIF) 可能是 APS 的关键调节因子。因此，在本实验中，我们分析了在 TRIF 敲除的情况下 APS 对脂多糖 (LPS) 感染的 Caco2 细胞的影响。通过使用 qRT-PCR 和流式细胞术方法，我们分别在转录和翻译水平上分析了基因表达。转录和翻译水平上的基因表达结果表明，LPS 可以激活 TLR4 下游的髓样分化因子 88 (MyD88)-TNF 受体相关因子 (TRAF) 途径，并诱导促炎细胞因子的高表达。然而，APS 可以有效抑制 LPS 诱导的炎症反应。然而，在 TRIF 敲除的情况下，APS 不能有效抑制 LPS 激活的 MyD88-TRAF6 途径以及促炎细胞因子的表达。综上所述，我们得出结论，APS 可以通过依赖于 TRIF 的方式拮抗 LPS 诱导的炎症反应。
