Luteolin Inhibits Retinal Neovascularization via Blockade of ROS Production

Abstract

Purpose: : To evaluate the effect of luteolin on retinal neovascularization in-vivo and in-vitro.

Methods: : OIR mice were used to assess the antiangiogenic effect of luteolin in-vivo. One eye was treated with single intravitreal injection of luteolin (1 µM ) on PN14 and contralateral eye served as control. Both Eyes were taken on PN17. Neovascularization was assessed with fluorescein angiography (FA) and the numbers of vascular lumens were counted on hematoxylin and eosin stained cross-sections. The effect of luteolin on tert-butyl-hydroperoxide (TBH) induced reactive oxygen species (ROS) production and vascular endothelial growth factor (VEGF) expression were evaluated in-vitro, using human renal microvascular endothelial cells (HRMECs).

Results: : In contrast to the control eyes, luteolin treated eyes showed significantly reduced neovascular tufts on FA and fewer neovascular lumens on cross-section. On flow cytometric analysis, TBH induced intracellular ROS production in HRMECs was significantly inhibited by luteolin treatment. VEGF mRNA level of HRMECs was also suppressed in luteolin treated group.

Conclusions: : These data suggest that the luteolin could significantly reduce the retinal neovascularization in the mouse model of OIR. Suppressed ROS production by luteolin which lead to the decreased VEGF expression might be a key mechanism of luteolin induced antiangiogenic effect.

Keywords: retinal neovascularization • neovascularization • drug toxicity/drug effects