Polyphenol-rich Aronia melanocarpa juice sustains eNOS activation through phosphorylation and expression via redox-sensitive pathways in endothelial cells

• Published in: Food science and biotechnology Vol. 33; no. 12; pp. 2865 - 2875
• Main Authors: Kim, Jong Hun, Choi, Min Sik, Auger, Cyril, Lee, Ki Won, Schini-Kerth, Valérie B.
• Format: Journal Article
• Language: English
• Published: Singapore Springer Nature Singapore 01.09.2024; Springer Nature B.V; Springer/Korean Society of Food Science and Technology; 한국식품과학회
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Aronia melanocarpa; Cardiovascular diseases; Cell activation; Chemistry; Chemistry and Materials Science; Endothelial cells; endothelial nitric oxide synthase; Enzyme inhibitors; Food Science; FOXO1 protein; FOXO3 protein; Gene silencing; Inactivation; juices; Kinases; Life Sciences; MAP kinase; mitogen-activated protein kinase; Nitric oxide; Nitric-oxide synthase; Nutrition; Pharmaceutical sciences; Pharmacology; Phosphorylation; Research Article; Transcription factors; Vascular system; 식품과학; Endothelial nitric oxide synthase; Reactive oxygen species; (Chokeberry) juice; Nitric oxide; Endothelial cells; Aronia melanocarpa (Chokeberry) juice
• ISSN: 1226-7708; 2092-6456; 2092-6456
• DOI: 10.1007/s10068-024-01546-8

A sustained formation of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS) is crucial to safeguard the vascular system against the development of cardiovascular diseases. This study investigated the prolonged phosphorylation and expression of eNOS induced by polyphenol-rich Aronia melanocarpa juice (AMJ), along with its underlying mechanisms. The findings revealed that AMJ triggered concentration- and time-dependent increases in eNOS phosphorylation and expression, leading to sustained NO production for 15 h. Investigations with various enzymes and inhibitors revealed that the effect of AMJ was associated with redox sensitivity, activating the PI3-kinase/Akt, JNK, and p38 MAPK pathways. These pathways led to the inactivation of transcription factors FoxO1 and FoxO3a through phosphorylation, relieving their repression on eNOS expression. Therefore, the capability of AMJ to consistently trigger prolonged eNOS phosphorylation and expression via complex redox-sensitive pathways highlights its potential for maintaining vascular health and preventing cardiovascular diseases.