scholarly journals Black soybean seed coat polyphenols promote nitric oxide production in the aorta through the Akt/eNOS pathway

2020 ◽  
Vol 10 (8) ◽  
pp. 330
Author(s):  
Chiaki Domae ◽  
Hitoshi Ashida ◽  
Yoko Yamashita
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Seed Coat ◽  
Vascular Endothelial Cells ◽  
Soybean Seed ◽  
No Production ◽  
Vascular Endothelial ◽  
Intestinal Epithelial ◽  
Black Soybean ◽  
Soybean Seed Coat

Background: Black soybean seed coat contains an abundance of flavan-3-ols and possesses various bioregulatory functions. Nitric oxide (NO) is produced by endothelial nitric oxide synthase (eNOS) in vascular endothelial cells and regulates vascular function through vasodilation and the inhibition of platelet aggregation in blood vessels. It has been reported that flavan-3-ols increase NO production, but many previous reports used a high concentration of flavan-3-ols. In the present study, we investigated the effect of flavan-3-ol-rich black soybean seed coat extract (BE) on NO production at a lower concentration that is close to the concentration after permeation through the monolayer of Caco-2 cells.Methods: Human umbilical vein endothelial cells (HUVEC) were incubated with BE, and then NO production in the medium and eNOS phosphorylation in the cells were examined. Intestinal epithelial Caco-2 cells on the upper side of a transwell filter were co-cultured with HUVEC on the basolateral compartment of the transwell apparatus. BE was added from the upper side, and the basolateral medium was collected to measure the concentration of NO and the content of flavan-3-ols. Furthermore, HUVEC were incubated with each flavan-3-ol in order to individuate the most effective compound in BE.Results: BE significantly increased NO production in the medium of HUVEC. When polyphenols in BE were removed from the basolateral medium by ethyl acetate extraction, increased NO production from HUVEC was not observed. Additionally, BE increased phosphorylation of eNOS and Akt in HUVEC. A portion of flavan-3-ols in BE had permeated through intestinal epithelial cells. Among the flavan-3-ols that had permeated, procyanidin C1 had the strongest effect on NO production in HUVEC at the concentration that had permeated the monolayer of Caco-2 cells. Procyanidin C1 (0.05 µM) also induced phosphorylation of eNOS and Akt in HUVEC without affecting the cAMP level. Conclusion: A portion of flavan-3-ols in BE directly promoted NO production through the Akt/eNOS pathway in vascular endothelial cells. These findings suggest that flavan-3-ols in the black soybean seed coat may contribute to improve the vascular function.Keywords: Black soybean seed coat polyphenols; NO; eNOS; Akt; vascular endothelial cells

scholarly journals Black soybean seed coat polyphenols promote nitric oxide production in the aorta through glucagon-like peptide-1 secretion from the intestinal cells

2019 ◽  
Vol 10 (12) ◽  
pp. 7875-7882 ◽  
Author(s):  
Chiaki Domae ◽  
Fumio Nanba ◽  
Toshinari Maruo ◽  
Toshio Suzuki ◽  
Hitoshi Ashida ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Seed Coat ◽  
Soybean Seed ◽  
Intestinal Cells ◽  
No Production ◽  
Nitric Oxide Production ◽  
Black Soybean ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Soybean Seed Coat

Black soybean seed coat polyphenols were reported to possess NO Production.

Abstract 153: Bile Acid Receptor TGR5 Agonism Represents Anti-inflammatory Effects via Stimulating Nitric Oxide Production in Vascular Endothelial Cells

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Taiki Kida ◽  
Yoshiki Tsubosaka ◽  
Masatoshi Hori ◽  
Hiroshi Ozaki ◽  
Takahisa Murata
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Bile Acids ◽  
Inflammatory Responses ◽  
Vascular Endothelial Cells ◽  
Lithocholic Acid ◽  
Signal Pathways ◽  
No Production ◽  
Vascular Endothelial ◽  
Anti Inflammatory

Objective TGR5, a membrane-bound, G-protein-coupled receptor for bile acids, is known to be involved in regulation of energy homeostasis and inflammation. However, little is known about the function of TGR5 in vascular endothelial cells. In the present study, we examined whether TGR5 agonism represents anti-inflammatory effects in vascular endothelial cells focusing on nitric oxide (NO) production. Methods and Results In human umbilical vein endothelial cells (HUVECs), treatment with taurolithocholic acid (TLCA), which has the highest affinity to TGR5 among various bile acids, significantly reduced tumor necrosis factor (TNF)-α-induced vascular cell adhesion molecule (VCAM)-1 protein expression and adhesion of human monocytes, U937. These effects were abrogated by a NO synthase (NOS) inhibitor, N G -Monomethyl-L-arginine (L-NMMA). In bovine aortic endothelial cells (BAECs), treatment with TLCA as well as lithocholic acid, which also has high affinity to TGR5, significantly increased the NO production. In contrast, deoxycholic acid and chenodeoxycholic acid, which possess low affinity to TGR5, did not affect the NO production. Gene depletion of TGR5 by siRNA transfection abolished TLCA-induced NO production in BAECs. TLCA-induced NO production was also observed in HUVECs measured as intracellular cGMP accumulation. We next investigated the signal pathways responsible for the TLCA-induced NO production in endothelial cells. Treatment with TLCA increased endothelial NOS (eNOS) ser1177 phosphorylation in HUVECs. This response was accompanied by increased Akt ser473 phosphorylation and intracellular Ca 2+ ([Ca 2+ ] i ). Treatment with phosphoinositide 3-kinase (PI3K) inhibitor, LY294002, or blockade of calcium channel with La 3+ , significantly decreased TLCA-induced eNOS ser1177 phosphorylation and subsequent NO production. Conclusion These results indicate that TGR5 agonism can mediate anti-inflammatory responses by suppressing VCAM-1 expression and monocytes adhesion to endothelial cells. This function is dependent on NO production via Akt activation and [Ca 2+ ] i increase.

Regulation of nitric oxide synthesis by oxygen in vascular endothelial cells

1997 ◽  
Vol 272 (6) ◽  
pp. L1161-L1166 ◽  
Author(s):  
A. R. Whorton ◽  
D. B. Simonds ◽  
C. A. Piantadosi
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Oxidation Products ◽  
No Oxidation ◽  
No Production ◽  
Vascular Endothelial ◽  
Intact Cells ◽  
Aortic Endothelial Cells ◽  
Basal Rate

Vascular endothelial cells synthesize nitric oxide (NO) in response to agonists that elevate cytosolic free Ca2+ concentrations. Once activated, NO synthase (NOS) requires arginine, NADPH, and O2 as cosubstrates. In this study, we investigated the role of O2 in regulating endothelial NOS activity in intact bovine aortic endothelial cells by measuring the rate of nitrite (NO2-) and nitrate (NO3-) production after conversion of NO2- to S-nitrosoglutathione before analysis or after reduction of NO2- and NO3- to NO using acidic vanadium chloride. The basal rate of NO2- production was 6.5 +/- 0.8 pmol.min-1.mg protein-1. Thapsigargin (TG, 1 microM) elevated free cytosolic Ca2+ concentration and increased the rate of NO2- synthesis. At maximal concentrations of TG, the rate of stimulated NO2- production was linear for at least 20 min and was eightfold higher than the basal rate (53.5 +/- 1.8 pmol.min-1.mg protein-1). Incubation of cells in gas mixtures chosen to produce PO2 values in the physiological range led to a progressive fall in the rate of TG-stimulated NO2- production, as O2 concentrations were reduced from that of room air. The half-maximal effective concentration for NO2- production by intact cells was found to occur at 38 Torr. PO2 values higher than that of room air did not lead to a change in the rate of TG-stimulated NO2- production. To confirm that measurement of NO2- accurately reflects total NO production, both NO2- plus NO3- were measured in buffer samples from cells incubated in either room air or N2. The sum of these NO oxidation products was inhibited similarly by hypoxia. These findings suggest that O2 is an important determinant of NOS activity in hypoxic tissues or in vascular beds such as the pulmonary arterial or fetal circulation where PO2 values in the range of 40 Torr are encountered normally.

Progesterone increases nitric oxide synthesis in human vascular endothelial cells through activation of membrane progesterone receptor-α

2015 ◽  
Vol 308 (10) ◽  
pp. E899-E911 ◽  
Author(s):  
Yefei Pang ◽  
Jing Dong ◽  
Peter Thomas
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Progesterone Receptor ◽  
Map Kinase ◽  
Plasma Membranes ◽  
Vascular Endothelial Cells ◽  
No Production ◽  
Vascular Endothelial ◽  
Enos Phosphorylation ◽  
20 Nm

Progesterone exerts beneficial effects on the human cardiovascular system by inducing rapid increases in nitric oxide (NO) production in vascular endothelial cells, but the receptors mediating these nongenomic progesterone actions remain unclear. Using human umbilical vein endothelial cells (HUVECs) as a model, we show that progesterone binds to plasma membranes of HUVECs with the characteristics of membrane progesterone receptors (mPRs). The selective mPR agonist Org OD 02-0 had high binding affinity for the progesterone receptor on HUVEC membranes, whereas nuclear PR (nPR) agonists R5020 and medroxyprogesterone acetate displayed low binding affinities. Immunocytochemical and Western blot analyses confirmed that mPRs are expressed in HUVECs and are localized on their plasma membranes. NO levels increased rapidly after treatment with 20 nM progesterone, Org OD 02-0, and a progesterone-BSA conjugate but not with R5020, suggesting that this progesterone action is at the cell surface and initiated through mPRs. Progesterone and Org OD 02-0 (20 nM) also significantly increased endothelial nitric oxide synthase (eNOS) activity and eNOS phosphorylation. Knockdown of mPRα expression by treatment with small-interfering RNA (siRNA) blocked the stimulatory effects of 20 nM progesterone on NO production and eNOS phosphorylation, whereas knockdown of nPR was ineffective. Treatment with PI3K/Akt and MAP kinase inhibitors blocked the stimulatory effects of progesterone, Org OD 02-0, and progesterone-BSA on NO production and eNOS phosphorylation and also prevented progesterone- and Org OD 02-0-induced increases in Akt and ERK phosphorylation. The results suggest that progesterone stimulation of NO production in HUVECs is mediated by mPRα and involves signaling through PI3K/Akt and MAP kinase pathways.

Hydroxytyrosol NO regulates oxidative stress and NO production through SIRT1 in diabetic mice and vascular endothelial cells

Phytomedicine ◽  
2019 ◽  
Vol 52 ◽  
pp. 206-215 ◽  
Author(s):  
Weirong Wang ◽  
Chenxu Shang ◽  
Wei Zhang ◽  
Zhen Jin ◽  
Feng Yao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
No Production ◽  
Vascular Endothelial ◽  
Diabetic Mice
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