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Mangiferin Protect Oxidative Stress Against Deoxynivalenol Induced Damages Through Nrf2 Signalling Pathways in Endothelial Cells

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Specialties Pharmacology
Physiology
Date 2020 Oct 30
PMID 33124065
Citations 6
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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.

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