Isolation, structural characterization of polysaccharide from Cephalosporium sinensis mycelia and its anti-nephritic effects in adenine-induced CKD rats.
Isolation, structural characterization of polysaccharide from Cephalosporium sinensis mycelia and its anti-nephritic effects in adenine-induced CKD rats.
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DOI：
10.1016/j.ijbiomac.2020.03.195
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发表时间：
2020-03
影响因子：
8.2
通讯作者：
Z. Zha;Zhijie Zhang;Weikun Wei;Wenbing Nie;W. Chu;Fengjie Huang;Long Yue;Su-Yan Wang;
中科院分区：
文献类型：
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作者：
Z. Zha;Zhijie Zhang;Weikun Wei;Wenbing Nie;W. Chu;Fengjie Huang;Long Yue;Su-Yan Wang;
从中华头孢霉菌丝体中分离纯化得到一种新的多糖（CSMP，分子量为16，685 Da）。单糖组成分析表明，CSMP由甘露糖、葡萄糖和半乳糖组成。详细的结构分析表明，CSMP具有由→ 2，6）-β-D-Manp-（1→和→ 3，6）-β-D-Manp-（1→），以及两个支链，包括α-D-Manp-（1→6）-α-D-Glcp-（1→和α-D-Glcp-（1→4）-α-D-Glcp-（1→3）-β-D-Galp-（1→2）-β-D-Manp-（1→连接到→ 2，6的C6上）-β-D-Manp-（1→和→ 3，6）-β-D-Manp-（1→。口服CSMP对腺嘌呤诱导的慢性肾脏病（CKD）大鼠具有肾脏保护作用。进一步分析表明，CSMP使乳杆菌属、球状梭菌属和双歧杆菌属的相对丰度增加，而使Echerichias亚群的相对丰度减少。CSMP增加结肠和盲肠中醋酸盐、丙酸盐和丁酸盐的水平。其机制可能与上调G蛋白偶联受体41（GPR 41）表达，下调核因子-κ B（NF-κB）水平，抑制组蛋白去乙酰化酶（HDAC）活性，提高调节性T细胞（Tcells）比例有关。这些结果表明，CSMP可被开发为治疗CKD的潜在药物之一。
In this study, a new polysaccharide (CSMP, Mw = 16,685 Da) was isolated and purified fromCephalosporium sinensismycelia. Monosaccharide composition analysis indicated that CSMP consists of mannose, glucose and galactose. A detailed structural analysis revealed that CSMP has a backbone consisting of →2,6)-β-D-Manp-(1→ and →3,6)-β-D-Manp-(1→, as well as two branched chains including of α-D-Manp-(1→6)-α-D-Glcp-(1→ and α-D-Glcp-(1→4)-α-D-Glcp-(1→3)-β-D-Galp-(1→2)-β-D-Manp-(1→ attached to C6 of →2,6)-β-D-Manp-(1→ and →3,6)-β-D-Manp-(1→. Orally administrated CSMP showed renal protection function in adenine-induced chronic kidney disease (CKD) rats. Further analysis demonstrated that CSMP increased relative abundance of the generaLactobacillusgroup,Clostridiumcoccoidesgroup andBifidobacterium, and decreasedEcherichiasubgroup. CSMP increased acetate, propionate and butyrate levels both in colon and cecum. The mechanisms behind these effects could be related to the down-regulation nuclear factor kappa-B (NF-κB) level by up-regulating expression of G protein-coupled receptor 41 (GPR41) and improvement regulatory T cells (Tregs) ratio by inhibiting histone deacetylase (HDAC) activity. These results indicated that CSMP could be developed as one of the potential drugs in the treatment of CKD.