Astragalus polysaccharides attenuated inflammation and balanced the gut microflora in mice challenged with Salmonella typhimurium
Astragalus polysaccharides attenuated inflammation and balanced the gut microflora in mice challenged with Salmonella typhimurium
复制标题
黄芪多糖减轻炎症并平衡肠道
DOI：
10.1016/j.intimp.2019.105681
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发表时间：
2019-09-01
影响因子：
5.6
通讯作者：
Li, Deshan
中科院分区：
文献类型：
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作者：
Dong, Na;Li, Xinran;Li, Deshan
鼠伤寒沙门氏菌（S. t）是引起急性胃肠炎的主要病原体之一。为探讨黄芪多糖（APS）的体内抗炎作用机制及其对肠道植物群的影响，以BALB/c小鼠感染S. t.建立腹泻模型。疾病活动指数（DAI）评分显示APS对S. t.-引起小鼠体重减轻和腹泻。黄芪多糖能显著降低肝、脾指数和血清ALT、AST水平（P < 0.05）。苏木精-伊红染色结果表明，黄芪多糖能显著增加空肠绒毛高度和隐窝深度，减少炎性细胞浸润（P < 0.05）。此外，APS还可增加空肠紧密连接蛋白ZO-1、Occludin和Claudin-1的表达水平。16 S rDNA分析结果表明，APS显著增加了乳酸杆菌和双歧杆菌的数量。正常水平（与对照组相比）。黄芪多糖还能显著降低空肠组织中促炎细胞因子TNF-α、IL-1 β、IL-6和IL-17的mRNA表达水平（P < 0.01）以及考克斯-2和iNOS的蛋白表达水平（P < 0.05）。Western blot证实，预先饲喂APS可抑制S。t. - 诱导空肠中TLR 4和MyD 88的表达，并进一步抑制核因子-κ B（NP-kappa B）活化，包括p65 NF-kappa B亚基的核转位以及IKB-α的磷酸化和降解。这是APS抑制空肠炎性因子和炎性介质产生的关键。
Salmonella typhimurium (S. t) is one of the main pathogens that causes acute gastroenteritis. To evaluate the anti-inflammatory mechanism of Astragalus polysaccharide (APS) in vivo and its influence on the intestinal flora, BALB/c mice were infected with S. t. to establish a model of diarrhea. The disease activity index (DAI) scores showed that APS attenuated S. t.-induced weight loss and diarrhea in mice. APS significantly reduced the index of the liver and spleen as well as the ALT and AST levels in serum (P < 0.05). Hematoxylin and eosin (H&E) results indicated that APS significantly increased jejunum villus height and crypt depth and reduced the infiltration of inflammatory cells (P < 0.05). Additionally, APS increased the tight junction (TJ) proteins expression levels of ZO-1, Occludin and Claudin-1 in the jejunum. The results of 16S rDNA showed that APS significantly increased the number of Lactobacillus and Bifidobacterium spp. to normal levels (compared with the control group). In addition, APS significantly decreased the mRNA expression levels of the proinflammatory cytokines TNF-alpha, IL-1 beta, IL-6 and IL-17 in the jejunum (P < 0.01) as well as the proteins expression levels of COX-2 and iNOS (P < 0.05). Western blot confirmed that prefeeding with APS inhibited S. t. -induced expression of TLR4 and MyD88 in the jejunum and further inhibited nuclear factor-KB (NP-kappa B) activation, including the nuclear translocation of the p65 NF-kappa B subunit and the phosphorylation and degradation of IKB-alpha. This was the key to APS inhibition of the production of inflammatory factors and inflammatory mediators in the jejunum.