| 발표일자: |
2013년 04월 20일 (토) |
| 발표시간: |
14:16~14:24 |
| 발표번호: |
망막F-027 |
| 발표장소: |
B방 |
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| 루테올린의 VEGF 발현 및 작용 억제를 통한 망막신생혈관 감소 효과 |
| 1 서울대학교병원 망막혈관실험실; 2 서울대학교 의과대학 안과학교실; 3 한국한의학연구원 한약연구본부 |
| 박성욱1, 조창식1, 전형오1, 류남희3, 김진형1, 유영석1, 2, 김진숙3, 김정훈1, 2 |
| 목적 : Oxidative stress-induced vascular endothelial growth factor (VEGF) is thought to play a critical role in the pathogenesis of retinopathy of prematurity (ROP). This study was to investigate the anti-angiogenic effect of luteolin against reactive oxygen species (ROS) induced retinal neovascularization.방법 : The toxicity of luteolin was evaluated through modified MTT assay in HRMECs as well as TUNEL assay in the retina of C57BL/6J. After intravitreal injection of luteolin in the mouse model of ROP, retinal neovascularization was examined by FAG and vessel counting. Anti-angiogenic activity of luteolin was evaluated by VEGF-induced migration and tube formation assay. The effect of luteolin on t-BH-induced ROS production was measured with DCFDA. The effect of luteolin on t-BH induced and hypoxia-induced VEGF transcription and expression were evaluated by RT-PCR and Western blot, respectively.결과 : Luteolin never affected the viability of HRMECs up to 10 μM, where luteolin never induce any structural change in all retinal layers. Luteolin inhibited retinal neovascularization in the mouse model of ROP. Moreover, VEGF-induced migration and tube formation were significantly decreased by co-treatment of luteolin. Luteolin attenuated VEGF transcription via blockade of t-BH induced ROS production. Luteolin suppressed hypoxia-induced VEGF expression via attenuating hypoxia inducible factor 1 α expression.결론 : Our results suggest that luteolin could be a potent anti-angiogenic agent for retinal neovascularization, which is related to anti-oxidative activity to block ROS production and to subsequently suppress VEGF expression and the pro-angiogenic effect of VEGF. |
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