Abstract
Purpose: :
N-Acetyl-cystein (NAC) is a potent anti-oxidant known as a glutathione precursor. The purpose of the present study was to investigate the role of NAC in the formation of choroidal neovascularization (CNV).
Methods: :
CNV was induced by laser photocoagulation of the ocular fundus in C57BL/6J mice. Mice were injected intraperitoneally with NAC or vehicle. The extent of CNV was evaluated by lectin staining. Macrophage recruitment after laser injury was determined by immunohistochemistry. The protein levels of monocyte chemotactic protein (MCP)-1, vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)-1, VEGFR-2 and C3a in the retinal pigment epithelium-choroid complex were examined by ELISA.
Results: :
The extent of CNV was significantly reduced in NAC-treated treatment mice compared with vehicle treated mice (P = 0.01). Furthermore, macrophage recruitment was significantly prevented in NAC-treated mice compared with vehicle-treated mice. (p < 0.001) The levels of MCP-1, VEGF, VEGFR-1 and VEGFR-2 were also significantly decreased in NAC-treated mice. (p = 0.008, 0.01, 0.03 and 0.02, respectively) However, the level of C3a was not suppressed by NAC treatment.
Conclusions: :
Our findings indicate that NAC inhibit the development of laser-induced CNV via macrophage infiltration but not complement activation, suggesting novel preventative and interventional therapeutic strategies for AMD.
Keywords: choroid: neovascularization • immunohistochemistry • antioxidants