scholarly journals Occludin downregulation in high glucose is regulated by SSTR2 via the VEGF/NRP1/Akt signaling pathway in RF/6A cells

2017 ◽  
Vol 14 (2) ◽  
pp. 1732-1738 ◽  
Author(s):  
Mengling Li ◽  
Shuaiwei Wang ◽  
Songjiang Wang ◽  
Lei Zhang ◽  
Dongdong Wu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
High Glucose ◽  
Akt Signaling ◽  
Akt Signaling Pathway

scholarly journals The PI3K/Akt Signaling Pathway Mediates the High Glucose-Induced Expression of Extracellular Matrix Molecules in Human Retinal Pigment Epithelial Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Dong Qin ◽  
Guo-ming Zhang ◽  
Xun Xu ◽  
Li-ya Wang
Keyword(s):  
Extracellular Matrix ◽  
Signaling Pathway ◽  
High Glucose ◽  
Retinal Pigment ◽  
Akt Signaling ◽  
Collagen Iv ◽  
Akt Signaling Pathway ◽  
Induced Expression ◽  
Rpe Cells ◽  
Extracellular Matrix Molecules

Prolonged hyperglycemia is an important risk factor of the pathogenesis of diabetic retinopathy (DR). Extracellular matrix molecules, such as fibronectin, collagen IV, and laminin, are associated with fibrotic membranes. In this study, we investigated the expression of fibronectin, collagen IV, and laminin in RPE cells under high glucose conditions. Furthermore, we also detected the phosphorylation of protein kinase B (Akt) under high glucose conditions in RPE cells. Our results showed that high glucose upregulated fibronectin, collagen IV, and laminin expression, and activated Akt in RPE cells. We also found that pretreatment with LY294002 (an inhibitor of phosphatidylinositol 3-kinase) abolished high glucose-induced expression of fibronectin, collagen IV, and laminin in RPE cells. Thus, high glucose induced the expression of fibronectin, collagen IV, and laminin through PI3K/Akt signaling pathway in RPE cells, and the PI3K/Akt signaling pathway may contribute to the formation of fibrotic membrane during the development of DR.

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.

High glucose induces alternative activation of macrophages via PI3K/Akt signaling pathway

2017 ◽  
Vol 37 (4) ◽  
pp. 409-415 ◽  
Author(s):  
Jie Wang ◽  
Jingjing Liu ◽  
Yuying Wang ◽  
Minghui Lin ◽  
Wei Tian ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
High Glucose ◽  
Akt Signaling ◽  
Alternative Activation ◽  
Akt Signaling Pathway

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 Metformin and asarone inhibit HepG2 cell proliferation in a high glucose environment by regulating AMPK and Akt signaling pathway

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Bhrigu Kumar Das ◽  
Rachel M. Knott ◽  
Pramod C. Gadad
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase ◽  
Signaling Pathway ◽  
Hepg2 Cell ◽  
High Glucose ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Morphological Changes ◽  
Akt Signaling ◽  
Dependent Manner ◽  
Akt Signaling Pathway

Abstract Background Metabolic dysregulation is one of the hallmarks of tumor cell proliferation. Evidence indicates the potential role of the 5′adenosine monophosphate-activated protein kinase (AMPK) and protein kinase B/Akt signaling pathway in regulating cell proliferation, survival, and apoptosis. The present study explores the effect of metformin HCl and the combination of α- and β-asarone on the proliferation of HepG2 cells in the presence of high glucose levels simulating the diabetic-hepatocellular carcinoma (HCC) condition. Results The metformin and asarone reduced HepG2 cell viability in a dose-dependent manner and induced morphological changes as indicated by methyl thiazolyl tetrazolium (MTT) assay. The metformin and asarone arrested the cells at the G0/G1 phase, upregulated the expression of AMPK, and downregulated Akt expression in high glucose conditions as identified by the flow cytometry technique. Further, the upregulated AMPK led to a decrease in the expression of phosphoenolpyruvate carboxykinase-2 (PCK-2) and sterol regulatory element-binding protein-1 (SREBP-1). Conclusion The anti-proliferative effect of metformin and asarone in the diabetic-HCC condition is mediated via AMPK and Akt pathway.

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