S-Space College of Medicine/School of Medicine (의과대학/대학원) Ophthalmology (안과학전공) Journal Papers (저널논문_안과학전공)
Homoisoflavanone inhibits retinal neovascularization through cell cycle arrest with decrease of cdc2 expression
- Kim, Jeong Hun; Kim, Ki Hyun; Kim, Jin Hyoung; Yu, Young Suk; Kim, Young-Myeong; Kim, Kyu-Won; Kwon, Ho Jeong
- Issue Date
- Academic Press
- Biochem Biophys Res Commun. 2007 Nov 3;362(4):848-52. Epub 2007 Aug 28.
- Animals; CDC2 Protein Kinase/*metabolism; Cell Cycle/drug effects; Disease Models, Animal; Dose-Response Relationship, Drug; Down-Regulation/drug effects; Humans; Infant, Newborn; Isoflavones/*therapeutic use; Mice; Mice, Inbred C57BL; Retinal Neovascularization/*drug therapy/*metabolism/pathology; Retinopathy of Prematurity/*drug therapy/*metabolism/pathology
- Neovascularization in the eye is the most common cause of blindness in all age groups; retinopathy of prematurity (ROP), diabetic retinopathy, and age-related macular degeneration. Despite current advances in surgical treatments, ROP remains as the most serious problem of vision loss in children. Here, we report that homoisoflavanone, a natural product from Cremastra appendiculata, significantly reduces retinal neovascularization in a mouse model of ROP. Homoisoflavanone inhibited the cell growth of HUVECs, but its cytotoxic effect was not observed in a concentration range of 1-20 microM. HUVECs population gradually increased in G2/M phase and reduced in G0/G1 and S phases after exposure to the compound. Homoisoflavanone decreased the level of cdc2 expression whereas the level of p21WAF1 expression was increased in a dose-dependent manner. These data demonstrate that homoisoflavanone could inhibit retinal neovascularization and be applied in the treatment of other vasoproliferative retinopathies.
- 0006-291X (Print)
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