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Last Updated: 3 years ago

Possible Interaction: Nitric Oxide and Epigallocatechin Gallate

Research Papers that Mention the Interaction

EGCG enhances the bioavailability of normal NO by reducing levels of the endogenous NO inhibitor asymmetric dimethylarginine.
Journal of cardiovascular pharmacology  •  2019  |  View Paper
In addition, EGCG caused vasorelaxation of rat aortic ring only partially abolished by a nitric oxide synthase inhibitor.
PloS one  •  2013  |  View Paper
Epigallocatechin gallate (EGCG), the major polyphenol in green tea, acutely stimulates production of nitric oxide ( NO ) from vascular endothelium to reduce hypertension and improve endothelial dysfunction in spontaneously hypertensive rats.
The Journal of nutritional biochemistry  •  2012  |  View Paper
The possible interference with the production of NO was also studied: both DCA and EGCG inhibited nitrite production in LPS-stimulated macrophages by 24% and 40%, respectively, and the expression of nitric oxide synthase-2 (NOS-2), as well.
Archives of biochemistry and biophysics  •  2008  |  View Paper
Thus, EGCG effectively mitigates cellular damage by lowering the inflammatory reaction and reducing the lipid peroxidation and NO generated radicals leading to the oxidative stress.
Cardiovascular & hematological disorders drug targets  •  2007  |  View Paper
Nitric oxide production was reduced by EGCG and black tea theaflavins by suppressing inducible nitric oxide synthase via blocking nuclear translocation of the transcription factor nuclear factor-kappaB as a result of decreased IkappaB kinase activity.
Anti-cancer agents in medicinal chemistry  •  2006  |  View Paper
We provide evidence that (−)‐epigallocatechin gallate (EGCG), a major monomer of green tea polyphenols, potently inhibits lipopolysaccharide (LPS)‐activated microglial secretion of nitric oxide ( NO ) and tumor necrosis factor‐α (TNF‐α) through the down‐regulation of inducible NO synthase and TNF‐α expression.
Journal of neuroscience research  •  2004  |  View Paper
In addition, EGCG enhanced the protein ratio of p-Akt/Akt, endothelial nitric oxide synthase (eNOS) activation and nitric oxide (NO) formation in injured cells.
Apoptosis  •  2017  |  View Paper
Our results showed that pre-treatment with EGCG could significantly reduce the production of TNF-α, Rantes, MCP-1, ICAM-1, NO , VEGF, and MMP-2 in LPS-stimulated L02 hepatocytes in a dose-dependent manner.
Acta biochimica et biophysica Sinica  •  2014  |  View Paper
In searching for the mechanism by which EGCG affects endothelial cells, we found that EGCG increases Akt phosphorylation, eNOS phosphorylation, and nitric oxide (NO) production.
NOS inhibition revealed that NO mediates the anti-inflammatory effects of EGCG.
Biological chemistry  •  2008  |  View Paper
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