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来自菌丝体的半乳葡聚糖在肝细胞中的结构表征及抗炎作用

Structural characterization and anti-inflammatory effect in hepatocytes of a galactoglucan from mycelium.

作者信息

Tang Huiling, Nie Wenbing, Xiao Jinna, Zha Zhengqi, Chen Qiuli, Yin Hongping

机构信息

School of Life Science and Technology, State Key Laboratory of Natural Medicines, China Pharmaceutical University No. 24 Tongjiaxiang Road Nanjing 210009 Jiangsu People's Republic of China

Department of Pharmacy, Jiangsu Food & Pharmaceutical Science College Huaian 223003 People's Republic of China.

出版信息

RSC Adv. 2019 Mar 8;9(14):7664-7672. doi: 10.1039/c8ra10347j. eCollection 2019 Mar 6.

DOI:10.1039/c8ra10347j
PMID:35521177
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9061278/
Abstract

The galactoglucan ACP2 was isolated from cultured mycelium through anion-exchange column chromatography and Sephadex G-100 chromatography and shown to exhibit hepatoprotective function in L02 cells. Based on monosaccharide composition analysis, ACP2 was mainly composed of glucose, galactose, and 6-deoxyglucose in a molar ratio of 5 : 2 : 1. The average molecular weight of ACP2 was 1.93 × 10 Da. The primary structure of ACP2 was elucidated with Fourier-transform infrared spectroscopy, gas chromatography-mass spectrometry, and nuclear magnetic resonance spectroscopy. The results indicated the following composition: →6)-linked-β-d-Gal-(1→, →6)-linked-α-d-Glc-(1→, →3)-linked-α-d-Glc-(1→, and →2,4)-linked-β-d-Glc-(1→, with terminal 6-deoxy-α-d-Glc and α-d-Glc. ACP2 alleviated lipopolysaccharide-induced hepatocyte inflammation by down-regulating the expressions of COX-2, IL-1β, TNF-α and IL-6. The decreased expressions of TLR4, MyD88, NF-κB, and phosphorylated p38 in ACP2-treated L02 cells indicated that ACP2 might ameliorate inflammation through the TLR4 and p38/NF-κB signaling pathways.

摘要

通过阴离子交换柱色谱法和葡聚糖G-100色谱法从培养的菌丝体中分离出半乳葡聚糖ACP2,并证明其在L02细胞中具有保肝功能。基于单糖组成分析,ACP2主要由葡萄糖、半乳糖和6-脱氧葡萄糖组成,摩尔比为5∶2∶1。ACP2的平均分子量为1.93×10 Da。采用傅里叶变换红外光谱、气相色谱-质谱和核磁共振光谱对ACP2的一级结构进行了阐明。结果表明其组成如下:→6)-连接-β-d-半乳糖-(1→、→6)-连接-α-d-葡萄糖-(1→、→3)-连接-α-d-葡萄糖-(1→和→2,4)-连接-β-d-葡萄糖-(1→,带有末端6-脱氧-α-d-葡萄糖和α-d-葡萄糖。ACP2通过下调COX-2、IL-1β、TNF-α和IL-6的表达减轻脂多糖诱导的肝细胞炎症。在ACP2处理的L02细胞中,TLR4、MyD88、NF-κB和磷酸化p38的表达降低,表明ACP2可能通过TLR4和p38/NF-κB信号通路改善炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed69/9061278/f91b7433913f/c8ra10347j-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed69/9061278/807a827e5479/c8ra10347j-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed69/9061278/9ed2aecdda68/c8ra10347j-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed69/9061278/ce9db173e1e3/c8ra10347j-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed69/9061278/f91b7433913f/c8ra10347j-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed69/9061278/807a827e5479/c8ra10347j-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed69/9061278/9ed2aecdda68/c8ra10347j-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed69/9061278/ce9db173e1e3/c8ra10347j-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed69/9061278/f91b7433913f/c8ra10347j-f4.jpg

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