Objective:

2

To investigate the inhibitory effects and underlying mechanisms of Qideng Mingmu Capsule (QD) on retinal neovascularization (RNV).

Methods:

2

Seven-day-old C57BL/6J mice were assigned to the following groups: control

oxygen-induced retinopathy (OIR)

low-

medium-

high-dose QD (225

450

and 900 mg/g daily)

and angiopoietin 1 (Ang1)

20 mice in each group. Except for the control group

an OIR model was induced by exposing mice to a hyperoxic environment for 5 d (postnatal days 7–12)

followed by a normoxic environment for 5 d (postnatal days 12–17). From day 12

the treatment groups received QD orally or Ang1 via binocular intravitreal injection. On day 17

hematoxylin and eosin staining and fluorescein isothiocyanate-dextran staining were performed to evaluate RNV growth. Immunofluorescence staining

immunohistochemistry

and Western blotting were used to analyze the expressions of Ang/tyrosine kinase with immunoglobulin and epidermal growth factor homology domain-2 (Tie2) signaling pathway

hypoxia-inducible factor-1α (HIF-1α)

and retinal vascular maturation markers. In addition

the effects of QD on the viability of rat retinal microvascular endothelial cells (rRMECs) was assessed.

Results:

2

QD significantly inhibited RNV formation

reduced RNV density

increased the expressions of Ang1

Tie2

and phosphorylated protein kinase B

and decreased the expression of Ang2 (

P

<

0.05 or

P

<

0.01). QD also enhanced retinal vascular pericyte coverage

reduced HIF-1α expression

and increased vascular endothelial cadherin levels (

P

<

0.05 or

P

<

0.01). Furthermore

no adverse effects were observed on the viability of rRMECs after QD intervention.

Conclusions:

2

QD effectively inhibited RNV formation

promoted neovascular maturation and remodeling

and protected retinal function by modulating the Ang/Tie2 signaling pathway. Therefore

QD may serve as a promising therapeutic option for retinal neovascular diseases.