Dihydromyricetin protects HUVECs of oxidative damage induced by sodium nitroprusside through activating PI3K/Akt/FoxO3a signalling pathway

Abstract

The damage of vascular endothelial cells induced by oxidative stress plays an important role in the pathogenesis of atherosclerosis. Dihydromyricetin (DMY) is considered as a natural antioxidant. However, the mechanism of DMY on endothelial cell injury induced by oxidative stress remains unclear. In this study, we found that DMY could reduce the oxidative damage of HUVECs induced by sodium nitroprusside (SNP), HUVECs pre‐treated with DMY suppressed SNP‐induced apoptosis by reduced ROS overproduction of intracellular, decreased MDA level and elevated the superoxide dismutase activity. Meanwhile, we found that DMY could promote the expression of phosphorylated FoxO3a and Akt, and affect the nuclear localization of FoxO3a, when treated with the PI3K inhibitor LY294002, the effect of DMY was blocked. These data suggest that DMY protects HUVECs from oxidative stress by activating PI3K/Akt/FoxO3a signalling pathway. Therefore, DMY may have great therapeutic potential as a new drug for atherosclerosis.

CLEC3B protects H9c2 cardiomyocytes from apoptosis caused by hypoxia via the PI3K/Akt pathway

“…Therefore, the PI3K/Akt pathway might be a potential target for the treatment of myocardial ischemia. Moreover, cleaved-caspase 3 is an apoptosis-activating protein, which is regulated by the PI3K/Akt pathway and serves as a marker for the apoptosis-promoting effect (27,28). Therefore, we conjectured that the effect of CLEC3B on the proliferation and apoptosis of hypoxic H9c2 cardiomyocytes might be connected with the PI3K/ Akt pathway and the expression of cleaved-caspase 3.…”

Dihydromyricetin Alleviates High Glucose-Induced Oxidative Stress and Apoptosis in Human Retinal Pigment Epithelial Cells by Downregulating miR-34a Expression

“… 33 DHM ameliorates oxidative stress and apoptotic damage of human umbilical vein endothelial cells induced by sodium nitroprusside. 18 It is noteworthy that DHM protects against diabetic cardiomyopathy and diabetic nephropathy. 21 , 22 In this study, the significant inhibitory effects of DHM on HG-induced oxidative stress and apoptosis in ARPE 19 cells was observed, suggesting the protective effects of DHM on DR.…”

“…14–17 A report demonstrated previously that DHM ameliorated oxidative stress and apoptotic damage of human umbilical vein endothelial cells induced by sodium nitroprusside. 18 Jiang et al found that DHM protected PC12 cells against oxidative stress response induced by methylglyoxal through regulating the AMPK/GLUT4 pathway. 19 Importantly, DHM enhanced glucose uptake in 3T3-L1 cells, and prevented the development of diabetic cardiomyopathy and diabetic nephropathy.…”

Down-Regulation of miR-301a-3p Reduces Burn-Induced Vascular Endothelial Apoptosis by potentiating hMSC-Secreted IGF-1 and PI3K/Akt/FOXO3a Pathway

“…These data confirmed miR-301a-3p negatively regulating hMSC-secreted IGF-1 reduced severe burn-induced vascular endothelial apoptosis via activating PI3K/Akt/FOXO3a signaling. And studies showed that phosphorylation of FOXOs by Akt inhibited transcriptional functions of FOXOs and contributed to cell survival, growth, and proliferation, thereby protecting against injured tissue or organ function ( Zhang et al., 2011 , 2019 ; Tucka et al., 2014 ). In addition, FOXO3 was also considered an evolutionarily conserved longevity factor, and FOXO3-activated vascular cells exhibited delayed aging and increased resistance to injury, even FOXO3-enhanced vascular cells could promote vascular regeneration in a mouse model of ischemic injury ( Flachsbart et al., 2017 ; Martins et al., 2016 ; Yan et al., 2019 ).…”