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云芝多糖通过抗氧化和抗炎活性缓解 PM 诱导的小鼠肺损伤。

Trametes orientalis polysaccharide alleviates PM-induced lung injury in mice through its antioxidant and anti-inflammatory activities.

机构信息

School of Food and Biological Engineering, Xuzhou University of Technology, Xuzhou 221018, China.

出版信息

Food Funct. 2019 Dec 11;10(12):8005-8015. doi: 10.1039/c9fo01777a.

DOI:10.1039/c9fo01777a
PMID:31763641
Abstract

This paper examined the molecular conformation of Trametes orientalis polysaccharide (TOP-2) and evaluated the ameliorative effects of TOP-2 on PM2.5-induced lung injury in mice. The Congo red test and transmission electron microscopy (TEM) showed that TOP-2 had a triple-helical structure. PM2.5-induced pulmonary edema was ameliorated by TOP-2 intervention. PM2.5 notably increased the number of inflammatory cells and percentages of neutrophils in bronchoalveolar lavage fluid (BALF), and notably reduced the percentages of macrophages in BALF, while TOP-2 abolished these effects. The increased levels of total protein, albumin, C-reactive protein (CRP), myeloperoxidase (MPO), lactate dehydrogenase (LDH), alkaline phosphatase (AKP), acid sphingomyelinase (ASM), TNF-α, IL-1β and IL-6 in BALF after PM2.5 exposure were inhibited by TOP-2. In addition, TOP-2 could not only remarkably promote the activities of antioxidant enzymes, but also reduce the levels of malondialdehyde (MDA), protein carbonyl group (PCG) and 8-hydroxy-2'-deoxyguanosine (8-OHdG). Furthermore, TOP-2 up-regulated the expressions of nuclear factor-erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) and inhibited the activation of NLR family pyrin domain-containing 3 (NLRP3) inflammasome in the lung tissue. These results hint that TOP-2 could alleviate PM2.5-induced lung injury in mice via its antioxidant and anti-inflammatory activities, and the underlying mechanisms, at least partly, depended on activation of the Nrf2/HO-1 pathway and inhibition of NLRP3 inflammasome.

摘要

本研究考察了云芝多糖(TOP-2)的分子构象,并评估了 TOP-2 对 PM2.5 诱导的小鼠肺损伤的改善作用。刚果红试验和透射电子显微镜(TEM)表明 TOP-2 具有三螺旋结构。TOP-2 干预可改善 PM2.5 诱导的肺水肿。PM2.5 显著增加了支气管肺泡灌洗液(BALF)中炎症细胞的数量和中性粒细胞的百分比,显著降低了 BALF 中巨噬细胞的百分比,而 TOP-2 消除了这些作用。TOP-2 抑制了 PM2.5 暴露后 BALF 中总蛋白、白蛋白、C 反应蛋白(CRP)、髓过氧化物酶(MPO)、乳酸脱氢酶(LDH)、碱性磷酸酶(AKP)、酸性鞘磷脂酶(ASM)、TNF-α、IL-1β 和 IL-6 水平的升高。此外,TOP-2 不仅能显著促进抗氧化酶的活性,还能降低丙二醛(MDA)、蛋白羰基(PCG)和 8-羟基-2'-脱氧鸟苷(8-OHdG)的水平。此外,TOP-2 上调了核因子-红细胞 2 相关因子 2(Nrf2)和血红素加氧酶-1(HO-1)的表达,并抑制了肺组织中 NLR 家族吡啶结构域包含 3(NLRP3)炎性体的激活。这些结果提示,TOP-2 通过其抗氧化和抗炎活性缓解 PM2.5 诱导的小鼠肺损伤,其潜在机制至少部分依赖于 Nrf2/HO-1 通路的激活和 NLRP3 炎性体的抑制。

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