State Key Laboratory of Biobased Material and Green Papermaking, Qilu University of Technology, Shandong Academy of Science, Jinan, 250353, P. R. China.
Shandong Provincial Key Laboratory of Microbial Engineering, Department of Bioengineering, Qilu University of Technology, Shandong Academy of Science, Jinan, 250353, P. R. China.
Food Funct. 2022 Apr 4;13(7):3946-3956. doi: 10.1039/d1fo03969e.
The effect of () on colitis and its underlying mechanism were rarely studied. In this study, 217-1 was used to ferment roots, and the concentrations of platycodin-D, flavonoids, and polyphenols and the DPPH free radical scavenging rate were significantly increased. Treatment with a root fermentation broth (PGRFB) could reduce dextran sulfate sodium (DSS) induced ulcerative colitis (UC) in mice. Meanwhile, the PGRFB significantly reduced the content of inflammatory factors in mouse serum and the expression of inflammatory factor mRNA in the intestinal tract, regulated the polarization of M1/M2 macrophages, and increased the expression of tight junction protein mRNA in intestinal epithelial cells. In summary, it was proved that the PGRFB could inhibit the nuclear factor kappa B (NF-κB) signaling pathway and the expression of Nod-like receptor protein 3 (NLRP3) inflammasomes by activating AMP-activated protein kinase (AMPK) and lowering the release of pro-inflammatory cytokines.
（）对结肠炎的影响及其作用机制鲜见研究。本研究采用 217-1 发酵 根，显著提高了远志酸-D、类黄酮和多酚的浓度和 DPPH 自由基清除率。用远志根发酵液（PGRFB）处理可减轻葡聚糖硫酸钠（DSS）诱导的小鼠溃疡性结肠炎（UC）。同时，PGRFB 显著降低了小鼠血清中炎症因子的含量和肠道中炎症因子 mRNA 的表达，调节了 M1/M2 巨噬细胞的极化，增加了肠道上皮细胞中紧密连接蛋白 mRNA 的表达。综上所述，证明 PGRFB 通过激活 AMP 激活的蛋白激酶（AMPK）和降低促炎细胞因子的释放，抑制核因子 kappa B（NF-κB）信号通路和 Nod 样受体蛋白 3（NLRP3）炎性小体的表达。
