PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20021702-6 2010 Of the nine other polyphenols tested, only epigallocatechin gallate had similar effects on both the eNOS and ET-1 mRNA expression, but to a lesser extent than resveratrol at an equimolar concentration (0.1 microm). epigallocatechin gallate 43-67 nitric oxide synthase 3 Homo sapiens 100-104 20117080-0 2010 The EGCg-induced redox-sensitive activation of endothelial nitric oxide synthase and relaxation are critically dependent on hydroxyl moieties. epigallocatechin gallate 4-8 nitric oxide synthase 3 Homo sapiens 47-80 19722703-8 2009 Concentration-dependent correlations between enhanced NO level and endothelial nitric oxide synthase (eNOS) expression were demonstrated for the three polyphenols tested (resveratrol, ECg, and EGCg). epigallocatechin gallate 193-197 nitric oxide synthase 3 Homo sapiens 67-100 33371812-7 2021 Besides, EGCG also restores homocysteine-mediated dephosphorylation of Akt and decreases endothelial NO synthase (eNOS) expression. epigallocatechin gallate 9-13 nitric oxide synthase 3 Homo sapiens 114-118 33371812-9 2021 The present study shows that EGCG prevents homocysteine-induced endothelial cell apoptosis via enhancing SIRT1/AMPK as well as Akt/eNOS signaling pathways. epigallocatechin gallate 29-33 nitric oxide synthase 3 Homo sapiens 131-135 32848435-0 2020 Erratum: (-)-Epigallocatechin-3-Gallate Inhibits eNOS Uncoupling and Alleviates High Glucose-Induced Dysfunction and Apoptosis of Human Umbilical Vein Endothelial Cells by PI3K/AKT/eNOS Pathway [Corrigendum]. epigallocatechin gallate 9-39 nitric oxide synthase 3 Homo sapiens 49-53 32848435-0 2020 Erratum: (-)-Epigallocatechin-3-Gallate Inhibits eNOS Uncoupling and Alleviates High Glucose-Induced Dysfunction and Apoptosis of Human Umbilical Vein Endothelial Cells by PI3K/AKT/eNOS Pathway [Corrigendum]. epigallocatechin gallate 9-39 nitric oxide synthase 3 Homo sapiens 181-185 32765028-0 2020 (-)-Epigallocatechin-3-Gallate Inhibits eNOS Uncoupling and Alleviates High Glucose-Induced Dysfunction and Apoptosis of Human Umbilical Vein Endothelial Cells by PI3K/AKT/eNOS Pathway. epigallocatechin gallate 0-30 nitric oxide synthase 3 Homo sapiens 40-44 32765028-0 2020 (-)-Epigallocatechin-3-Gallate Inhibits eNOS Uncoupling and Alleviates High Glucose-Induced Dysfunction and Apoptosis of Human Umbilical Vein Endothelial Cells by PI3K/AKT/eNOS Pathway. epigallocatechin gallate 0-30 nitric oxide synthase 3 Homo sapiens 172-176 32765028-13 2020 Conclusion: EGCG could inhibit eNOS uncoupling and alleviate endothelial dysfunction and apoptosis of HG-treated HUVECs by activating the PI3K/AKT/eNOS pathway. epigallocatechin gallate 12-16 nitric oxide synthase 3 Homo sapiens 31-35 32765028-13 2020 Conclusion: EGCG could inhibit eNOS uncoupling and alleviate endothelial dysfunction and apoptosis of HG-treated HUVECs by activating the PI3K/AKT/eNOS pathway. epigallocatechin gallate 12-16 nitric oxide synthase 3 Homo sapiens 147-151 32173528-4 2020 Green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) directly binds to cell-surface 67LR and induces apoptosis through the protein kinase B (Akt)/endothelial nitric oxide synthase/nitric oxide/cyclic GMP (cGMP) axis. epigallocatechin gallate 21-53 nitric oxide synthase 3 Homo sapiens 154-187 32173528-4 2020 Green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) directly binds to cell-surface 67LR and induces apoptosis through the protein kinase B (Akt)/endothelial nitric oxide synthase/nitric oxide/cyclic GMP (cGMP) axis. epigallocatechin gallate 55-59 nitric oxide synthase 3 Homo sapiens 154-187 28317089-0 2017 EGCG protects against homocysteine-induced human umbilical vein endothelial cells apoptosis by modulating mitochondrial-dependent apoptotic signaling and PI3K/Akt/eNOS signaling pathways. epigallocatechin gallate 0-4 nitric oxide synthase 3 Homo sapiens 163-167 28317089-8 2017 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. epigallocatechin gallate 13-17 nitric oxide synthase 3 Homo sapiens 59-92 28317089-8 2017 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. epigallocatechin gallate 13-17 nitric oxide synthase 3 Homo sapiens 94-98 28317089-9 2017 In conclusion, the present study shows that EGCG prevents Hcy-induced HUVECs apoptosis via modulating mitochondrial apoptotic and PI3K/Akt/eNOS signaling pathways. epigallocatechin gallate 44-48 nitric oxide synthase 3 Homo sapiens 139-143 25581901-0 2015 Transient receptor potential vanilloid type 1 is vital for (-)-epigallocatechin-3-gallate mediated activation of endothelial nitric oxide synthase. epigallocatechin gallate 59-89 nitric oxide synthase 3 Homo sapiens 113-146 23567873-8 2013 EGCG inhibited 7KC-induced monocytic adhesion to endothelial cells, and induced expression of eNOS and several genes involved in the CaMKKII pathway. epigallocatechin gallate 0-4 nitric oxide synthase 3 Homo sapiens 94-98 23567873-9 2013 Stimulation of endothelial cells with EGCG produced intracellular ROS, whereas treatment with N-acetylcysteine (NAC) blocked EGCG-induced expression of eNOS and CaMKKII. epigallocatechin gallate 125-129 nitric oxide synthase 3 Homo sapiens 152-156 23104077-1 2013 (-)-Epigallocatechin-3-O-gallate (EGCg) has been shown to induce endothelium-dependent nitric oxide (NO)-mediated relaxation via the redox-sensitive Src/PI3-kinase/Akt-dependent phosphorylation of endothelial NO synthase (eNOS). epigallocatechin gallate 0-32 nitric oxide synthase 3 Homo sapiens 222-226 23104077-1 2013 (-)-Epigallocatechin-3-O-gallate (EGCg) has been shown to induce endothelium-dependent nitric oxide (NO)-mediated relaxation via the redox-sensitive Src/PI3-kinase/Akt-dependent phosphorylation of endothelial NO synthase (eNOS). epigallocatechin gallate 34-38 nitric oxide synthase 3 Homo sapiens 222-226 23104077-2 2013 Although the presence of 8 hydroxyl functions, mainly on B and D rings, is essential for the EGCg-induced activation of eNOS, the relative role of each individual hydroxyl function still remains unclear. epigallocatechin gallate 93-97 nitric oxide synthase 3 Homo sapiens 120-124 23104077-3 2013 This study examined the effect of selective replacement of hydroxyl functions by methoxy moieties on either the B or D ring on the EGCg-induced phosphorylation of Akt and eNOS, formation of reactive oxygen species (ROS) and NO in cultured coronary artery endothelial cells, and endothelium-dependent relaxation of coronary artery rings. epigallocatechin gallate 131-135 nitric oxide synthase 3 Homo sapiens 171-175 23104077-6 2013 These findings suggest that the hydroxyl group at the 3"" position of the gallate ring is essential and, also, to some extent, the two hydroxyl groups at positions 3" and 4", for the EGCg-induced redox-sensitive activation of eNOS leading to the subsequent NO-mediated vascular relaxation. epigallocatechin gallate 183-187 nitric oxide synthase 3 Homo sapiens 226-230