PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26939766-7 2016 But vascular permeability, VEGF, and COX-2 expressions were reduced in animals treated with the resveratrol group compared with the cabergoline group (group 5) and the severe OHSS (group 3) group. Resveratrol 96-107 vascular endothelial growth factor A Rattus norvegicus 27-31 29880170-6 2018 Peritoneal fluid VEGF levels were lower for RSV group compared to group 2 and 3. Resveratrol 44-47 vascular endothelial growth factor A Rattus norvegicus 17-21 29880170-8 2018 CONCLUSION: These results indicate that RSV is beneficial for prevention of OHSS by reducing the increases in body and ovarian weight and VEGF activity. Resveratrol 40-43 vascular endothelial growth factor A Rattus norvegicus 138-142 29875625-0 2018 Resveratrol Promotes Nerve Regeneration via Activation of p300 Acetyltransferase-Mediated VEGF Signaling in a Rat Model of Sciatic Nerve Crush Injury. Resveratrol 0-11 vascular endothelial growth factor A Rattus norvegicus 90-94 29875625-9 2018 Resveratrol activated p300 acetyltransferase-mediated VEGF signaling in the affected ventral spinal cord, which may have thus contributed to the acceleration of nerve regeneration and motor repair. Resveratrol 0-11 vascular endothelial growth factor A Rattus norvegicus 54-58 29434758-8 2018 Resveratrol significantly increased the expression of eNOS (P<0.01) and suppressed the expression of VEGF and p-p38 (both P<0.01) in rats with DRMI. Resveratrol 0-11 vascular endothelial growth factor A Rattus norvegicus 104-108 29434758-9 2018 These results suggest that treatment with resveratrol is able to improve cardiovascular function via inhibition of eNOS and VEGF, and suppression of p38 phosphorylation in rats with DRMI. Resveratrol 42-53 vascular endothelial growth factor A Rattus norvegicus 124-128 29037554-8 2017 RESULTS: Histological evaluation and immunohistochemical evaluations showed that treatment with a resveratrol significantly increased the thickness of the uterine wall and VEGF expression and decreased expression PDGF during wound healing. Resveratrol 98-109 vascular endothelial growth factor A Rattus norvegicus 172-176 26939766-9 2016 CONCLUSION(S): Our results in a rat model suggest that resveratrol has a beneficial effect on OHSS by reducing the increases in ovarian daimeter, VP, and VEGF expression associated with OHSS. Resveratrol 55-66 vascular endothelial growth factor A Rattus norvegicus 154-158 25373440-5 2015 Serum VEGF (p = 0.05) and MCP-1 (p = 0.01) levels after treatment were also significantly lower in the resveratrol and leuprolide acetate groups. Resveratrol 103-114 vascular endothelial growth factor A Rattus norvegicus 6-10 25295523-0 2014 The suppressive effect of resveratrol on HIF-1alpha and VEGF expression after warm ischemia and reperfusion in rat liver. Resveratrol 26-37 vascular endothelial growth factor A Rattus norvegicus 56-60 25295523-2 2014 The aim of the present study was to investigate the effect of resveratrol (RES) on the expression of ischemic-induced HIF-1alpha and vascular endothelial growth factor (VEGF) in rat liver. Resveratrol 62-73 vascular endothelial growth factor A Rattus norvegicus 133-167 25295523-2 2014 The aim of the present study was to investigate the effect of resveratrol (RES) on the expression of ischemic-induced HIF-1alpha and vascular endothelial growth factor (VEGF) in rat liver. Resveratrol 62-73 vascular endothelial growth factor A Rattus norvegicus 169-173 24312656-11 2013 Increased permeability and cellular junction disruption of cultured endothelial cells caused by VEGF were also inhibited by resveratrol pretreatment. Resveratrol 124-135 vascular endothelial growth factor A Rattus norvegicus 96-100 22148982-0 2012 Effect of resveratrol on Bcl-2 and VEGF expression in oxygen-induced retinopathy of prematurity. Resveratrol 10-21 vascular endothelial growth factor A Rattus norvegicus 35-39 22959450-10 2012 However, resveratrol decreased aromatization and VEGF expression, whereas AMH expression remained unaltered. Resveratrol 9-20 vascular endothelial growth factor A Rattus norvegicus 49-53 22148982-9 2012 Significant differences in expression of Bcl-2 and VEGF were also noted among the three treatment groups with resveratrol (P < .01). Resveratrol 110-121 vascular endothelial growth factor A Rattus norvegicus 51-55 22148982-10 2012 After treatment with resveratrol at 10, 30, and 60 mg/kg/d, the inhibition rate of Bcl-2 expression was 11.1%, 38.1%, and 69.8% and that of VEGF expression was 3.4%, 23.0%, and 43.7%, respectively. Resveratrol 21-32 vascular endothelial growth factor A Rattus norvegicus 140-144 22148982-11 2012 CONCLUSION: Resveratrol can significantly inhibit expression of Bcl-2 and VEGF in the retina of neonatal rats with oxygen-induced ROP. Resveratrol 12-23 vascular endothelial growth factor A Rattus norvegicus 74-78 21574020-5 2011 Resveratrol (10 nM) or N-acetylcysteine (NAC, 20 mM) diminished the transcriptional activity of hypoxiainducible factor-1 and hypoxia-induced expression of VEGF. Resveratrol 0-11 vascular endothelial growth factor A Rattus norvegicus 156-160 22191573-2 2012 The present study investigated the effects of resveratrol (RSV) treatment on the mRNA expression profile of VEGF, ACE, MMP-9, and eNOS, which are associated with vascular neovascularization, and glutathione, protein carbonyl, and nitrite-nitrate levels, which are markers of oxidative stress in eyes of diabetic rats. Resveratrol 46-57 vascular endothelial growth factor A Rattus norvegicus 108-112 22191573-2 2012 The present study investigated the effects of resveratrol (RSV) treatment on the mRNA expression profile of VEGF, ACE, MMP-9, and eNOS, which are associated with vascular neovascularization, and glutathione, protein carbonyl, and nitrite-nitrate levels, which are markers of oxidative stress in eyes of diabetic rats. Resveratrol 59-62 vascular endothelial growth factor A Rattus norvegicus 108-112 17664136-9 2007 Resveratrol produced significant induction of p-AKT, p-eNOS, Trx-1, HO-1, and VEGF in addition to increased activation of MnSOD activity in diabetic animals compared to nondiabetic animals. Resveratrol 0-11 vascular endothelial growth factor A Rattus norvegicus 78-82 17664136-11 2007 In the present study we found that the mechanism(s) responsible for the cardioprotective effect of resveratrol in the diabetic myocardium include upregulation of Trx-1, NO/HO-1, and VEGF in addition to increased MnSOD activity and reduced blood glucose level. Resveratrol 99-110 vascular endothelial growth factor A Rattus norvegicus 182-186 16456233-0 2006 Resveratrol ameliorates myocardial damage by inducing vascular endothelial growth factor-angiogenesis and tyrosine kinase receptor Flk-1. Resveratrol 0-11 vascular endothelial growth factor A Rattus norvegicus 54-88 16456233-5 2006 We have successfully demonstrated in rat myocardial infarction (MI) model an effect of resveratrol on significant upregulation of the protein expression profiles of vascular endothelial growth factor (VEGF) and its tyrosine kinase receptor Flk-1, 3 wk after MI. Resveratrol 87-98 vascular endothelial growth factor A Rattus norvegicus 165-199 16456233-5 2006 We have successfully demonstrated in rat myocardial infarction (MI) model an effect of resveratrol on significant upregulation of the protein expression profiles of vascular endothelial growth factor (VEGF) and its tyrosine kinase receptor Flk-1, 3 wk after MI. Resveratrol 87-98 vascular endothelial growth factor A Rattus norvegicus 201-205 33472443-2 2021 Resveratrol is a highly effective anti-VEGF agent against CNV. Resveratrol 0-11 vascular endothelial growth factor A Rattus norvegicus 39-43 16198371-3 2005 Here we report resveratrol enhanced myocardial angiogenesis both in vivo and in vitro by induction of vascular endothelial growth factor (VEGF), which was regulated by thioredoxin-1 (Trx-1) and heme oxygenase-1 (HO-1). Resveratrol 15-26 vascular endothelial growth factor A Rattus norvegicus 102-136 16198371-3 2005 Here we report resveratrol enhanced myocardial angiogenesis both in vivo and in vitro by induction of vascular endothelial growth factor (VEGF), which was regulated by thioredoxin-1 (Trx-1) and heme oxygenase-1 (HO-1). Resveratrol 15-26 vascular endothelial growth factor A Rattus norvegicus 138-142 16198371-7 2005 Again, rat neonatal cardiomyocytes treated with resveratrol significantly expressed Trx-1, HO-1 as well as VEGF. Resveratrol 48-59 vascular endothelial growth factor A Rattus norvegicus 107-111 16198371-10 2005 Concomitantly, resveratrol-treated myocardium after MI significantly induced Trx-1, HO-1 and VEGF expression. Resveratrol 15-26 vascular endothelial growth factor A Rattus norvegicus 93-97 16198371-12 2005 Our findings suggest that resveratrol mediates cardioprotection and neovascularization through Trx-1-HO-1-VEGF pathway in rat ischemic myocardium. Resveratrol 26-37 vascular endothelial growth factor A Rattus norvegicus 106-110 15905131-0 2005 Coordinated induction of iNOS-VEGF-KDR-eNOS after resveratrol consumption: a potential mechanism for resveratrol preconditioning of the heart. Resveratrol 50-61 vascular endothelial growth factor A Rattus norvegicus 30-34 15905131-0 2005 Coordinated induction of iNOS-VEGF-KDR-eNOS after resveratrol consumption: a potential mechanism for resveratrol preconditioning of the heart. Resveratrol 101-112 vascular endothelial growth factor A Rattus norvegicus 30-34 15905131-5 2005 Western blot detected an overexpression of iNOS and VEGF within 24 h of resveratrol treatment while the induction of KDR was not increased until after 3 days and eNOS expression after 5 days of resveratrol treatment. Resveratrol 72-83 vascular endothelial growth factor A Rattus norvegicus 52-56 15905131-9 2005 The hearts obtained from resveratrol-treated rats revealed enhanced expression for iNOS, eNOS and VEGF and KDR compared to control hearts at the end of reperfusion. Resveratrol 25-36 vascular endothelial growth factor A Rattus norvegicus 98-102 15905131-10 2005 The results of this study demonstrate that resveratrol leads to a coordinated upregulation of iNOS-VEGF-KDR-eNOS, which is likely to play a role in resveratrol-mediated cardioprotection. Resveratrol 43-54 vascular endothelial growth factor A Rattus norvegicus 99-103 15905131-10 2005 The results of this study demonstrate that resveratrol leads to a coordinated upregulation of iNOS-VEGF-KDR-eNOS, which is likely to play a role in resveratrol-mediated cardioprotection. Resveratrol 148-159 vascular endothelial growth factor A Rattus norvegicus 99-103 16198371-0 2005 Resveratrol enhances neovascularization in the infarcted rat myocardium through the induction of thioredoxin-1, heme oxygenase-1 and vascular endothelial growth factor. Resveratrol 0-11 vascular endothelial growth factor A Rattus norvegicus 133-167 30503749-5 2019 In an in vivo study, resveratrol significantly recovered the insulin level and PON1 expression and activity, as well as clearly reduced the retinal vascular permeability, retinal AGEs, LDL, Ox-LDL, caspase3 activity, retinal damage, IL-1beta, IL-6, TNFalpha, VEGF, IFNgamma and MCP-1 in STZ-diabetic rats. Resveratrol 21-32 vascular endothelial growth factor A Rattus norvegicus 259-263 33628394-10 2021 Results: Resveratrol can significantly decrease the expression of lipase, amylase, acetyl-FOXO1, VEGF, Ang II, ET, NO, TXB2, and 6-keto-PGF1alpha and the ratio of wet/dry weight, ET/NO, and TXB2/6-keto-PGF1alpha by improving microcirculatory dysfunction and blood viscosity in SAP. Resveratrol 9-20 vascular endothelial growth factor A Rattus norvegicus 97-101 32801741-0 2020 Resveratrol Suppresses Tumor Progression via Inhibiting STAT3/HIF-1alpha/VEGF Pathway in an Orthotopic Rat Model of Non-Small-Cell Lung Cancer (NSCLC). Resveratrol 0-11 vascular endothelial growth factor A Rattus norvegicus 73-77 32801741-2 2020 The aim of the present study was to investigate whether resveratrol (RES) could suppress NSCLC progression via inhibiting the expressions of STAT3, HIF-1alpha, and VEGF in a nude rat model. Resveratrol 56-67 vascular endothelial growth factor A Rattus norvegicus 164-168 32801741-2 2020 The aim of the present study was to investigate whether resveratrol (RES) could suppress NSCLC progression via inhibiting the expressions of STAT3, HIF-1alpha, and VEGF in a nude rat model. Resveratrol 69-72 vascular endothelial growth factor A Rattus norvegicus 164-168 30787995-6 2019 In addition, Rev upregulated the expression of MMP9, VEGF, and Cadherin5, indicating that Rev promotes angiogenesis in ischemic flaps. Resveratrol 13-16 vascular endothelial growth factor A Rattus norvegicus 53-57