Polysaccharide of Hericium erinaceus attenuates colitis in C57BL/6 mice via regulation of oxidative stress, inflammation-related signaling pathways and modulating the composition of the gut microbiota
Polysaccharide of Hericium erinaceus attenuates colitis in C57BL/6 mice via regulation of oxidative stress, inflammation-related signaling pathways and modulating the composition of the gut microbiota
复制标题
猴头菇多糖通过调节氧化应激、炎症相关信号通路和调节肠道微生物群的组成来减轻 C57BL/6 小鼠的结肠炎
DOI：
10.1016/j.jnutbio.2018.03.005
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发表时间：
2018-07-01
影响因子：
5.6
通讯作者：
Xu, Zheng-Hong
中科院分区：
文献类型：
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作者：
Ren, Yilin;Geng, Yan;Xu, Zheng-Hong
炎症性肠病（IBD）是一种病因不明的由免疫系统失调引起的疾病。猴头菌（Hericium erinaceus）是一种中药材真菌，具有预防和治疗胃肠道疾病的作用。本研究在葡聚糖硫酸钠（DSS）诱导的C57BL/6小鼠结肠炎模型中，检测了蛇尾多糖（HECP，分子量：86.67 kDa）的抗炎作用。我们的数据表明，HECP可以改善临床症状并下调氧化应激的关键标志物，包括一氧化氮（NO）、丙二醛（MDA）、总超氧化物歧化酶（T-SOD）和髓过氧化物酶（MPO）。hep还能抑制白细胞介素(IL)-6、白细胞介素(IL)-1 β、肿瘤坏死因子(TNF)- α的分泌，抑制环氧化酶-2 （COX-2）、诱导型一氧化氮合酶（iNOS）的表达，降低相关mRNA的表达。同时，HECP阻断dss处理小鼠核因子- kb (NF-kB) p65、NF-kB抑制剂α (ikb - α)、丝裂原活化蛋白激酶（MAPK）和蛋白激酶B （Akt）的磷酸化。此外，HECP逆转了dss诱导的肠道生态失调，维持了肠道屏障的完整性。综上所述，HECP可改善dss诱导的小鼠肠道损伤，提示HECP可作为抗IBD的保护性膳食营养素。(C) 2018年Elsevier Inc.出版
Inflammatory bowel disease (IBD) is a disease caused by a dysregulated immune with unknown etiology. Hericium erinaceus (H. erinaceus) is a Chinese medicinal fungus, with the effect of prevention and treatment of gastrointestinal disorders. In this study, we have tested the anti-inflammatory effect of polysaccharide of H. erinaceus (HECP, Mw: 86.67 kDa) in the model of dextran sulfate sodium (DSS)-induced colitis in C57BL/6 mice. Our data indicated that HECP could improve clinical symptoms and down-regulate key markers of oxidative stresses, including nitric oxide (NO), malondialdehyde (MDA), total superoxide dismutase (T-SOD), and myeloperoxidase (MPO). HECP also suppressed the secretion of interleukin (IL)-6, interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha and the expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and decreased the expression of related mRNA. Meanwhile, HECP blocked phosphorylation of nuclear factor-KB (NF-kB) p65, NF-kB inhibitor alpha (iKB-alpha), mitogen-activated protein kinases (MAPK) and Protein kinase B (Akt) in DSS-treated mice. Moreover, HECP reversed DSS-induced gut dysbiosis and maintained intestinal barrier integrity. In conclusion, HECP ameliorates DSS-induced intestinal injury in mice, which suggests that HECP can serve as a protective dietary nutrient against IBD. (C) 2018 Published by Elsevier Inc.