Biochem Biophys Res Commun 2008,
PMID: 18789310
Chung, Byung-Hee; Kim, Jong-Dai; Kim, Chun-Ki; Kim, Jung Hwan; Kim, Jung Huan; Won, Moo-Ho; Lee, Han-Soo; Dong, Mi-Sook; Ha, Kwon-Soo; Kwon, Young-Geun; Kim, Young-Myeong
We investigated the molecular effect and signal pathway of icariin, a major flavonoid of Epimedium koreanum Nakai, on angiogenesis. Icariin stimulated in vitro endothelial cell proliferation, migration, and tubulogenesis, which are typical phenomena of angiogenesis, as well as increased in vivo angiogenesis. Icariin activated the angiogenic signal modulators, ERK, phosphatidylinositol 3-kinase (PI3K), Akt, and endothelial nitric oxide synthase (eNOS), and increased NO production, without affecting VEGF expression, indicating that icariin may directly stimulate angiogenesis. Icariin-induced ERK activation and angiogenic events were significantly inhibited by the MEK inhibitor PD98059, without affecting Akt and eNOS phosphorylation. The PI3K inhibitor Wortmannin suppressed icariin-mediated angiogenesis and Akt and eNOS activation without affecting ERK phosphorylation. Moreover, the NOS inhibitor NMA partially reduced the angiogenic activity of icariin. These results suggest that icariin stimulated angiogenesis by activating the MEK/ERK- and PI3K/Akt/eNOS-dependent signal pathways and may be a useful drug for angiogenic therapy.
Diseases/Pathways annotated by Medline MESH: MAP Kinase Signaling System
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Text Mining Data
Akt → PI3K: "
The
PI3K inhibitor Wortmannin
suppressed icariin mediated angiogenesis and
Akt and eNOS activation without affecting ERK phosphorylation
"
eNOS → PI3K: "
The PI3K inhibitor Wortmannin suppressed icariin mediated angiogenesis and Akt and eNOS activation without affecting ERK phosphorylation
"
Manually curated Databases
No curated data.