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基于 iTRAQ 分析的 TLR4/MyD88/NF-κB 通路探讨黑灵芝多糖对丙烯酰胺致小鼠肠道屏障功能损伤的保护作用。

The protective effect of Ganoderma atrum polysaccharide on intestinal barrier function damage induced by acrylamide in mice through TLR4/MyD88/NF-κB based on the iTRAQ analysis.

机构信息

State Key Laboratory of Food Science and Technology, Nanchang University, 235 Nanjing East Road, Nanchang, 330047, People's Republic of China.

State Key Laboratory of Food Science and Technology, Nanchang University, 235 Nanjing East Road, Nanchang, 330047, People's Republic of China.

出版信息

Food Chem Toxicol. 2023 Jan;171:113548. doi: 10.1016/j.fct.2022.113548. Epub 2022 Dec 9.

Abstract

The potential mechanism for the protective effect of Ganoderma atrum (G. atrum) polysaccharide (PSG-1) on acrylamide (AA) induced intestinal damage in mice was explored. Results showed that PSG-1 pretreatment prevented AA-induced injury by decreasing intestinal permeability and serum D-lactate acid (D-Lac) levels and increasing the number of small intestinal goblet cells and IgA secreting cells. In addition, PSG-1 pretreatment effectively reduced malondialdehyde (MDA) level and raised superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) activities in the intestine. Furthermore, PSG-1 administration decreased the levels of pro-inflammatory factors including IL-1β, TNF-α, and IL-6, while the anti-inflammatory factor IL-10 was elevated. Meanwhile, PSG-1 could increase the performance of tight junction (TJ) proteins such as Occludin, Claudin-1 and ZO-1. Moreover, according to the isobaric tag for relative and absolute quantitation (iTRAQ) and Western blot results, PSG-1 could reduce AA-induced intestinal injury through TLR4/MyD88/NF-κB signaling pathway. Overall, the present study suggested that PSG-1 protected intestinal permeability and barrier function in mice via reducing inflammation and oxidative stress, and effectively prevented AA-induced intestinal injury in mice.

摘要

本研究旨在探索灵芝多糖(PSG-1)对丙烯酰胺(AA)诱导的小鼠肠道损伤的保护作用机制。结果表明,PSG-1 预处理可通过降低肠道通透性和血清 D-乳酸(D-Lac)水平,增加小肠杯状细胞和 IgA 分泌细胞数量,从而预防 AA 诱导的损伤。此外,PSG-1 预处理还能有效降低丙二醛(MDA)水平,提高超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽(GSH)活性。此外,PSG-1 给药可降低包括 IL-1β、TNF-α和 IL-6 在内的促炎因子水平,同时升高抗炎因子 IL-10。同时,PSG-1 可以增加紧密连接(TJ)蛋白如 Occludin、Claudin-1 和 ZO-1 的表达。此外,根据同位素标记相对和绝对定量(iTRAQ)和 Western blot 结果,PSG-1 可通过 TLR4/MyD88/NF-κB 信号通路减轻 AA 诱导的肠道损伤。综上所述,本研究表明 PSG-1 通过减轻炎症和氧化应激,保护小鼠肠道通透性和屏障功能,有效预防 AA 诱导的小鼠肠道损伤。

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