scholarly journals Antioxidant Blueberry Anthocyanins Induce Vasodilation via PI3K/Akt Signaling Pathway in High-Glucose-Induced Human Umbilical Vein Endothelial Cells

2020 ◽  
Vol 21 (5) ◽  
pp. 1575 ◽  
Author(s):  
Wuyang Huang ◽  
Ruth Paulina Hutabarat ◽  
Zhi Chai ◽  
Tiesong Zheng ◽  
Weimin Zhang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
High Glucose ◽  
Umbilical Vein ◽  
Akt Signaling ◽  
Ros Generation ◽  
Heme Oxygenase 1 ◽  
Peroxisome Proliferator ◽  
Akt Signaling Pathway ◽  
Peroxisome Proliferator Activated Receptor

Blueberries are rich in antioxidant anthocyanins. The hypotensive effects of blueberry anthocyanins in endothelial cells was investigated here. Pretreatment with blueberry anthocyanin extract, malvidin, malvidin-3-glucoside, and malvidin-3-galactoside significantly ameliorated high-glucose-induced damage by enhancing endogenous antioxidant superoxide dismutase (SOD) and heme oxygenase-1 (HO-1), lowering reactive oxygen species (ROS) generation and NADPH oxidase isoform 4 (NOX4) expression, and increasing the cell vitalities. They also effectively induced a vasodilatory effect by increasing the vasodilator nitric oxide (NO) and its promoters endothelial NO synthase (eNOS) and peroxisome proliferator-activated receptor-γ (PPARγ) levels as well as by decreasing the vasoconstrictor angiotensin-converting enzyme (ACE), xanthine oxidase-1 (XO-1), and low-density lipoprotein (LDL) levels. The activation of phosphoinositide 3-kinase (PI3K)/Akt signaling pathway and the breakdown of protein kinase C zeta (PKCζ) pathway were involved in the bioactivities. The results indicated blueberry anthocyanins protected endothelial function against high-glucose (HG) injury via antioxidant and vasodilatory mechanisms, which could be promising molecules as a hypotensive nutraceutical for diabetes patients.

scholarly journals The Effect and Mechanism of Emodin on the NO Secretion of Human Umbilical Vein Endothelial Cells (HUVECs) Induced by High Glucose

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Yajia Li ◽  
Qiangxiang Li ◽  
Chunyan Xie ◽  
Yanfei Huang ◽  
Limin Jia
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Signaling Pathway ◽  
High Glucose ◽  
Umbilical Vein ◽  
Akt Signaling ◽  
High Dose ◽  
Akt Signaling Pathway ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Objective. To investigate the effects of emodin on nitric oxide (NO) secretion induced by high glucose in human umbilical vein endothelial cells (HUVECs) through the p-Akt signaling pathway. Methods. Sensitivity of cells to emodin was determined by MTT assay to establish the experimental concentrations; then, HUVECs were treated with high-dose (33.3 mmol/L) glucose (HG), HG + emodin (HG + E), HG + the Akt phosphorylation inhibitor LY294002 (HG + LY), or HG + E + LY. The p-Akt (Ser 473) expression in 48 h was analyzed using Western blot. NO effect on the secretion of HUVECs was analyzed using nitrate reductase assay. Results. The sensitive emodin concentration for HUVECs growth was 10 mol/L (P<0.05). Compared with the HG group, NO secretion was significantly higher in the HG + E group (P<0.05), whereas it was lowest in the HG + LY group (P<0.05). Compared with the HG + LY group, NO secretion was increased in the HG + E + LY group (P<0.05). The p-Akt protein expression was decreased in the HG + LY group when compared to the HG group (P<0.05), while it significantly increased in the HG + E group (P<0.05). Compared with HG + LY group, p-Akt protein expression was significantly higher in the HG + E + LY group (P<0.05). Conclusion. Emodin could improve the NO secretion of HUVECs by high glucose through the p-Akt signaling pathway.

scholarly journals The inhibition of Bax activation-induced apoptosis by RasGRP2 via R-Ras-PI3K-Akt signaling pathway in the endothelial cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jun-ichi Takino ◽  
Takuma Sato ◽  
Kentaro Nagamine ◽  
Takamitsu Hori
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Akt Signaling ◽  
Ros Production ◽  
Nucleotide Exchange ◽  
Akt Signaling Pathway ◽  
Phosphoinositide 3 Kinase ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

Abstract Apoptosis of endothelial cells is a very important event in various diseases and angiogenesis. We recently reported that ras guanyl nucleotide releasing protein 2 (RasGRP2), which is a guanine nucleotide exchange factor, was expressed in the human umbilical vein endothelial cells (HUVECs) and that Rap1 activation by its overexpression inhibited apoptosis by suppressing tumor necrosis factor-α induced-reactive oxygen species (ROS) production. However, other signaling pathways and roles of RasGRP2 not mediated via Rap1 are not well understood. Therefore, we compared the Mock (M) and the RasGRP2-stable overexpression (R) immortalized HUVECs using BAM7 and anisomycin, which are apoptosis inducers. BAM7 and anisomycin induced apoptosis without causing ROS production, and such apoptosis was significantly increased in M cells, but not in R cells. RasGRP2 suppressed BAM7- and anisomycin-induced apoptosis, but not via the Rap1 pathway as observed using Rap1 knockdown. Furthermore, RasGRP2 activated not only Rap1 but also R-Ras, and suppressed apoptosis by activating R-Ras-phosphoinositide 3-kinase (PI3K)-Akt signaling pathway. The phosphorylation of Akt by RasGRP2 inhibited Bax translocation by promoting translocation of hexokinase-2 (HK-2) from cytoplasm to mitochondria. Taken together, it was suggested that RasGRP2 suppresses the Bax activation-induced apoptosis by promoting HK-2 translocation to mitochondria via R-Ras-PI3K-Akt signaling pathway.

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