HG (30 mM) exposed PC12 cells demonstrated reduced mitochondrial complex activities and oxygen consumption rate (OCR), decreased the expressions of Sirt1, peroxisome proliferator-activated receptor coactivator-1α (PGC1α), nuclear respiratory factor-2 (NRF2), LONP1 and ATP synthase c. SRT1720 treatment (4 μM) significantly reversed these effects in hyperglycemia insulted PC12 cells but silencing the expression of LONP1 impeded this effect of SRT1720 on mitochondrial complex activities, OCR and mitochondrial membrane potential.
<i>In vitro</i> experiments in rat macrophages showed that hyperglycemia treatment suppresses Nrf2 activation, resulting in oxidative stress with decreased expression of antioxidant genes, including NAD(P)H:quinone oxidoreductase 1 and heme oxygenase 1, together with increased secretion of proinflammatory cytokines, including interleukin 1β (IL1β), IL6, and monocyte chemoattractant protein-1.
Pharmacologic or systemic genetic activation of the Nrf2 pathway partially protects from obesity in mice and ameliorates fasting hyperglycemia in mice and humans.
Taken together, the endothelial protective effect of Baicalin under hyperglycemia condition could be partly attributed to its role in downregulating reactive oxygen species (ROS) and inflammation via the Akt/GSK3B/Fyn-mediated Nrf2 activation.
Cellular experiments indicate that Nrf2 expression inhibits hyperglycemia-induced apoptosis and promotes angiogenesis by regulating the TLR4/NFκB signal pathway.
In conclusion, PPAR<i>β</i>/<i>δ</i> activation confers vascular protection against hyperglycemia-induced oxidative stress by suppressing NOX-2 and NOX-4 expression plus a direct induction of HO-1; with the subsequent downregulation of the Nrf2 pathway.
<b>Conclusion:</b> The results of our study show the hypoglycemic impact of black truffle on STZ-induced hyperglycemia in rats via Nrf2 and NF-κB pathways, and both pathways have significant improvement that may support the hypoglycemic impact of truffle.
Gene knockdown of PHLPP1 in NRK52E cells enhanced Nrf2-responsive antioxidant enzymes HO-1 and NQO-1 which suggested that PHLPP1 up-regulation during hyperglycemia lowers Nrf2 stability via GSK3β activation.
In this study, HepG2 cells have been used to investigate the toxic effects of hyperglycemia and/or quercetin (Q) on mammalian target of rapamycin (m-TOR) and nuclear factor erythroid 2-related factor 2 (Nrf-2) expression as central molecules involved in cancer.
Green tea epigallocatechin 3-gallate alleviates hyperglycemia and reduces advanced glycation end products via nrf2 pathway in mice with high fat diet-induced obesity.
These results indicate that ASP maintains cellular homeostasis and protects the myocardium against hyperglycemia-induced oxidative stress through activation of <i>Nrf2</i> and its downstream target genes.
Effects of C-Glycosides from Apios americana Leaves against Oxidative Stress during Hyperglycemia through Regulating Mitogen-Activated Protein Kinases and Nuclear Factor Erythroid 2-Related Factor 2.
Nrf2/ARE signaling pathway is a crucial cellular defense system to cope with oxidative stress, which is adaptively activated, in diabetic condition that is not efficient enough to resist the oxidative stress provoked by hyperglycemia.
Taken together, the data suggest that Nrf2-modulated antioxidant stress plays a crucial role in maternal hyperglycaemia-induced neurodevelopmental defects.
The effect of hyperglycemia on H3K4 methylation in Nrf2 binding at Gclc-ARE4 was investigated by chromatin immunoprecipitation in the rat retina and was confirmed in retinal endothelial cells in which histone demethylase (LSD1) was manipulated.
Compared with wild-type mice, mice lacking Nrf2 (Nrf2-null) have lower basal serum insulin and prolonged hyperglycemia in response to an intraperitoneal glucose challenge.
The aim of this study was to assess whether activation of nrf2 by sulforaphane in human microvascular endothelial cells prevents metabolic dysfunction in hyperglycemia.