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. Author manuscript; available in PMC: 2019 Jul 17.
Published in final edited form as: Microvasc Res. 2018 Apr 7;119:29–37. doi: 10.1016/j.mvr.2018.03.011

Fig. 1.

Fig. 1.

Mab2F1 and H1L1 Inhibit Corneal Neovascularization (NV) and Opacity Induced by Alkali Burn. A–F: Representative images of the cornea on day 8 after alkali burn. A: Normal cornea without alkali burn; B: Alkali burn without treatment; C: Alkali burn with non-specific mouse IgG treatment; D: Alkali burn with Mab2F1 treatment; E: Alkali burn with non-specific human IgG treatment; F: Alkali burn with H1L1 treatment. White arrow indicated initial vessels boundary of corneal limbus; black arrow indicated corneal NV. G: Quantification of corneal NV areas on days 4, 6 and 8 after the injury. H: Quantification of the inflammatory index on days 4, 6 and 8 after the injury. Data were presented as Mean ± SEM (n = 6 per group) and analyzed by One-way analysis of variance test, followed by the Bonferroni post hoc analysis to compare the differences between the two groups. **P < 0.01, versus alkali-burn without treatment group; ## P < 0.01, Mab2F1 group versus mouse IgG group; ξξ P < 0.01, H1L1 group versus human IgG group.