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Updated: Mar 9, 2026
A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
Antiangiogenic Effects of Doxazosin on Experimental Choroidal Neovascularization in Mice
Jiaxian Guo1,2, Xueting Luo1,2, Jian Liang1,2
11 Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai, China .
Purpose:
The present study was designed to evaluate the effects of doxazosin on experimental choroidal neovascularization (CNV) in mice.
Methods:
Six- to 8-week-old male C57BL/6 mice were divided into a control group and a doxazosin-treated group (5 mg/kg, i.p., daily). Experimental CNV was induced by laser photocoagulation. Seven and 14 days after laser induction, fluorescein angiography, choroidal flat mounts, and histological studies were performed to evaluate the fluorescence leakage, area, and thickness of CNV lesions, respectively. In addition, western blot analysis was carried out to assess the inhibitory effects of doxazosin on the PI3K/Akt/mTOR signaling pathway and the expression levels of hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF), which are involved in CNV model.
Results:
Compared with the control group, the doxazosin-treated group demonstrated significantly less fluorescence leakage on day 7 and 14 after laser induction. Both the area and the thickness of CNV lesions in the doxazosin-treated group were significantly decreased. Mechanistically, PI3K/Akt/mTOR signaling pathway activation was significantly suppressed in the doxazosin-treated group. The expression of HIF-1α and VEGF was also notably reduced by systemic doxazosin treatment.
Conclusions:
Doxazosin exerts antiangiogenic actions in an experimental mouse model of CNV and may be a potential adjunctive therapy for neovascular age-related macular degeneration in humans.
Insights
Doxazosin significantly reduced choroidal neovascularization (CNV) in mice by inhibiting key signaling pathways. This suggests doxazosin may be a potential treatment for neovascular age-related macular degeneration.
Area of Science:
- Ophthalmology
- Angiogenesis Research
- Pharmacology
Background:
- Choroidal neovascularization (CNV) is a major cause of vision loss in age-related macular degeneration.
- Current therapies for CNV have limitations, necessitating the exploration of novel treatment strategies.
Purpose of the Study:
- To investigate the antiangiogenic effects of doxazosin in an experimental mouse model of CNV.
- To elucidate the molecular mechanisms underlying doxazosin's action on CNV.
Main Methods:
- Experimental CNV was induced in C57BL/6 mice via laser photocoagulation.
- Mice received daily intraperitoneal injections of doxazosin (5 mg/kg).
- CNV lesion size, leakage, and thickness were assessed using fluorescein angiography, choroidal flat mounts, and histology. Western blot analysis evaluated the PI3K/Akt/mTOR pathway, HIF-1α, and VEGF expression.
Main Results:
- Doxazosin treatment significantly reduced CNV lesion leakage, area, and thickness compared to controls.
- Systemic administration of doxazosin suppressed the PI3K/Akt/mTOR signaling pathway.
- Doxazosin treatment notably decreased the expression of hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF).
Conclusions:
- Doxazosin demonstrates significant antiangiogenic properties in a mouse model of CNV.
- The drug's mechanism involves the inhibition of the PI3K/Akt/mTOR pathway and downstream factors like HIF-1α and VEGF.
- Doxazosin holds potential as an adjunctive therapy for neovascular age-related macular degeneration in humans.
