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Protocatechuic Acid Induces Angiogenesis through P I3 K ‐ A kt‐e NOS ‐ VEGF Signalling Pathway
Author(s) -
Kang Zechun,
Zhu Haibo,
Jiang Wanglin,
Zhang Shuping
Publication year - 2013
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.12094
Subject(s) - angiogenesis , enos , protocatechuic acid , ly294002 , pi3k/akt/mtor pathway , protein kinase b , vascular endothelial growth factor , chemistry , vascular endothelial growth factor a , pharmacology , biology , cancer research , signal transduction , biochemistry , nitric oxide , nitric oxide synthase , endocrinology , vegf receptors , antioxidant
In this study, we sought to elucidate whether protocatechuic acid contributes to induce angiogenesis as well as its mechanisms. To this end, we examined the role of protocatechuic acid on human brain microvascular endothelial cell line ( HBMEC ) proliferation, invasion and tube formation in in vitro . For the study of mechanisms involved, the phosphoinositide 3 kinase (PI3K)‐Akt inhibitor LY 294002, the endothelial nitric oxide synthase ( eNOS ) inhibitor L ‐ NAME , vascular endothelial growth factor ( VEGF ), antagonist sF lt‐1 and VEGF receptor blocker SU ‐1498 were used. Proliferation of HBMEC was tested by MTT . Scratch adhesion test was used to assess the ability of invasion. A M atrigel tube formation assay was performed to test capillary tube formation ability. P I3K‐Akt‐ eNOS ‐ VEGF pathway activation in HBMEC was tested by W estern blot. Our data suggested that protocatechuic acid induces angiogenesis in vitro by increasing proliferation, invasion and tube formation. VEGF expression was increasing by protocatechuic acid and counteracted by VEGF antagonist sF lt‐1, LY 294002 and L‐ NAME in HBMEC . Tube formation was increased by protocatechuic acid and counteracted by VEGF receptor blocker‐ SU 1498, LY 294002 and L‐ NAME . These data suggest that protocatechuic acid may be a candidate therapy for stroke recovery by promoting angiogenesis via a programmed P I3K/Akt/ eNOS / VEGF signalling axis.