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Involvement of androgen receptor in nitric oxide production induced by icariin in human umbilical vein endothelial cells
Author(s) -
Koizumi Hideki,
Yu Jing,
Hashimoto Ryo,
Ouchi Yasuyoshi,
Okabe Tetsuro
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.04.049
Subject(s) - icariin , enos , wortmannin , umbilical vein , mapk/erk pathway , chemistry , phosphorylation , protein kinase b , pi3k/akt/mtor pathway , endocrinology , kinase , medicine , nitric oxide , nitric oxide synthase , pharmacology , microbiology and biotechnology , signal transduction , biochemistry , biology , in vitro , alternative medicine , pathology
Icariin, a flavonoid isolated from Epimedii herba , stimulated phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177, Akt (Ser473) and ERK1/2 (Thr202/Tyr204). The icariin‐induced eNOS phosphorylation was abolished by an androgen receptor (AR) antagonist, nilutamide in human umbilical vein endothelial cells (HUVECs). Furthermore, it was also reduced in the cells transfected with small interfering RNA in which the expression of AR was broken down. The icariin‐induced eNOS phosphorylation was inhibited by wortmannin, a phosphatidylinositol 3‐kinase (PI3K) inhibitor and partially attenuated by PD98059, an upstream inhibitor for ERK1/2. These data suggest that icariin stimulates release of NO by AR‐dependent activation of eNOS in HUVECs. PI3K/Akt and MAPK‐ERK kinase (MEK)/ERK1/2 pathways were involved in the phosphorylation of eNOS by icariin.