作者: Xi-Lin Lu , Jun-Xiu Liu , Qi Wu , Si-Mei Long , Min-Ying Zheng
DOI: 10.1016/J.EJPHAR.2014.03.030
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摘要: Abstract As40-induced vascular dysfunction has been implicated in the pathogenesis of Alzheimer׳s disease (AD). In present study, we investigated possible protective effects puerarin against damage and impairment to angiogenesis transgenic TG (fli1:EGFP) zebrafish human endothelial cells. As40 peptides at 5 μM caused an obvious reduction vessel branches subintestinal vein basket, induced NADPH oxidase-derived reactive oxygen species impaired growth factor (VEGF)-dependent angiogenesis. Pretreatment with attenuated Aβ40-induced a dose-dependent manner. addition, decreased VEGF-dependent phosphorylation Akt eNOS, whereas treatment these detrimental effects. Furthermore, restoration As40-induced-angiogenesis by was abolished either PI3 kinase inhibitor LY294002 (10 μM) or eNOS L-NAME. The study suggests that exerts its action probably through overproduction activation PI3K/Akt/eNOS pathways.