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Effect of minocycline on vascular proliferation after corneal alkaline burn: A mechanism study

Haijun Wu, Xin Dai, Hui Li, Chunying Lv

Impairment of vision or blindness always occurs in the progress of Corneal Neovascularization (CNV). CNV may cause corneal graft rejection at corneal transplant status. Thus, intervention of CNV is of concern to clinical treatment. Given minocycline was reported with inhibiting effect on CNV, our study was focused on specific effect of minocycline on CNV after corneal alkaline burn. Seventy five male Sprague Dawley rats (12 w old) were randomly and equally assigned into three groups, receiving Phosphate-Buffered Saline (PBS) (control group), 60 mg/kg or 30 mg/kg minocycline, respectively. Sodium hydroxide (NaOH) solution was used to establish corneal alkaline burn rat model, which were performed on left eyes of experimental rats. Vascular cover area of corneal hyperplasia was assessed for three groups at 5 d, 10 d and 15 d after corneal alkaline burn, respectively. Vascular proliferation was analysed for three groups. Expressions of VEGF and VEGFR were examined with qRT-PCR at 15 d after corneal alkaline burn. HUVECs were cultured with different concentration of minocycline. HUVECs proliferation, AKT and phosphorylation level of ERK1/2 were assessed in vitro, respectively. Compared with control group, CNV area was significantly decreased in minocycline treated groups (p<0.05). qRT-PCR showed that expressions of VEGF and VEGFR were inhibited by minocycline treatment. Cell experiment on HUVECS demonstrated that proliferation was inhibited after minocycline treatment, and such inhibiting effect was dose-dependent. In addition, minocycline decreased expression of AKT, and reduced phosphorylation level of ERK1/2. Minocycline inhibited vascular proliferation of CNV after alkaline burn via down-regulating multiple factors, including VEGF, VEGFR, AKT and phosphorylation level of ERK1/2.