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一种黑灵芝多糖通过保护凋亡/自噬调节的物理屏障和树突状细胞相关免疫屏障减轻葡聚糖硫酸钠诱导的溃疡性结肠炎。

A Ganoderma atrum polysaccharide alleviated DSS-induced ulcerative colitis by protecting the apoptosis/autophagy-regulated physical barrier and the DC-related immune barrier.

作者信息

Zheng Bing, Ying Mengxi, Xie Jianhua, Chen Yi, Wang Yudan, Ding Xiaomeng, Hong Jiaqian, Liao Wang, Yu Qiang

机构信息

State Key Laboratory of Food Science and Technology, China-Canada Joint Lab of Food Science and Technology (Nanchang), Nanchang University, 235 Nanjing East Road, Nanchang, 330047, China.

出版信息

Food Funct. 2020 Dec 1;11(12):10690-10699. doi: 10.1039/d0fo02260h. Epub 2020 Nov 21.

Abstract

Polysaccharides are one of the main active substances in Ganoderma atrum (G. atrum). The purpose of this study was to explore the protective effect of a G. atrum polysaccharide (PSG-1) on DSS-induced colitis and the underlying mechanism. The results showed that PSG-1 could maintain the integrity of the intestinal structure by promoting the expression of goblet cells and levels of tight junction proteins in the colon of DSS-induced colitis mice. Furthermore, PSG-1 relieved the inhibition of Bcl-2 and the overexpression of caspase-3 and caspase-9 caused by DSS. Simultaneously, PSG-1 restored the expression of Atg5, Atg7 and beclin-1 and inhibited the p-akt and p-mTOR levels, suggesting that PSG-1 promoted autophagy via the Akt/mTOR pathway. Moreover, PSG-1 inhibited the content of DCs in the colon and modulated the expression of IL-10 in DCs. In conclusion, PSG-1 alleviated DSS-induced ulcerative colitis by protecting the apoptosis/autophagy-regulated physical barrier and the DC-related immune barrier.

摘要

多糖是黑灵芝中的主要活性物质之一。本研究旨在探讨黑灵芝多糖(PSG-1)对葡聚糖硫酸钠(DSS)诱导的结肠炎的保护作用及其潜在机制。结果表明,PSG-1可通过促进DSS诱导的结肠炎小鼠结肠中杯状细胞的表达和紧密连接蛋白水平来维持肠道结构的完整性。此外,PSG-1减轻了DSS引起的Bcl-2抑制以及caspase-3和caspase-9的过表达。同时,PSG-1恢复了Atg5、Atg7和beclin-1的表达,并抑制了p-akt和p-mTOR水平,表明PSG-1通过Akt/mTOR途径促进自噬。此外,PSG-1抑制结肠中树突状细胞(DCs)的含量,并调节DCs中白细胞介素-10(IL-10)的表达。总之,PSG-1通过保护凋亡/自噬调节的物理屏障和DC相关的免疫屏障减轻了DSS诱导的溃疡性结肠炎。

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