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芒果苷通过 Nrf2 信号通路保护氧化应激对抗脱氧雪腐镰刀菌烯醇诱导的内皮细胞损伤。

Mangiferin protect oxidative stress against deoxynivalenol induced damages through Nrf2 signalling pathways in endothelial cells.

机构信息

Department of Nuclear Medicine, Faculty of Medicine, Kuwait University, Safat, Kuwait.

出版信息

Clin Exp Pharmacol Physiol. 2021 Mar;48(3):389-400. doi: 10.1111/1440-1681.13432. Epub 2020 Nov 12.

Abstract

Several cereal grains contain a mycotoxin food contaminant called deoxynivalenol (DON), which presents a significant health risk as it is one of the most commonly found mycotoxins. The current paper examines the ameliorative effect of mangiferin (MAN) in vascular endothelial cells induced through activating the Nrf2 signalling pathway on dietary DON-induced oxidative changes. The study infers that the intercellular reactive oxygen species (ROS) levels and malondialdehyde decrease due to MAN. Other effects include in human umbilical vein endothelial cells (HUVECs), the oxidative stress-induced cell damage is reduced due to protective effects and superoxide dismutase (SOD), and catalase (CAT) activities also reveal an improvement. In HUVECs, the Nrf2-regulated antioxidant enzyme genes' expression is activated by Nrf2 nuclear translocation induction and this activity suppresses the oxidative stress damage. The genes in HUVECs include HO-1 and NQO1. Moreover, in HUVECs, the nucleus translocation of Nrf2 reduces the Nrf2, HO-1, whereas NQO1 expression decreases the cytoprotective effects against oxidative stress reduce with the rejection of Nrf2 with siRNA. This paper pioneers in inferring that oxidative stress-induced HUVECs' cell injury is suppressed by MAN through Nrf2, signalling pathway activation.

摘要

几种谷物都含有一种真菌毒素食品污染物,叫做脱氧雪腐镰刀菌烯醇(DON),这是一种非常常见的真菌毒素,对健康构成了重大威胁。本文研究了芒果苷(MAN)通过激活 Nrf2 信号通路对膳食 DON 诱导的氧化变化的血管内皮细胞的改善作用。研究推断,由于 MAN 的作用,细胞间活性氧(ROS)水平和丙二醛降低。其他作用还包括在人脐静脉内皮细胞(HUVEC)中,由于保护作用和超氧化物歧化酶(SOD)以及过氧化氢酶(CAT)活性的提高,氧化应激诱导的细胞损伤减少。在 HUVEC 中,Nrf2 核转位诱导激活了 Nrf2 调节的抗氧化酶基因的表达,从而抑制了氧化应激损伤。这些基因包括 HO-1 和 NQO1。此外,在 HUVEC 中,Nrf2 的核转位减少了 Nrf2、HO-1,而 NQO1 的表达减少了细胞保护作用,对抗氧化应激的损伤随着 Nrf2 与 siRNA 的排斥而降低。本文首次推断,MAN 通过 Nrf2 信号通路的激活抑制了氧化应激诱导的 HUVEC 细胞损伤。

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