AIM: To investigate the effect of recombinant canstatin proteins with different concentration on the expressions of matrix metalloproteinase-2(MMP-2)and tissue inhibitor of metalloproteinase-2(TIMP-2)in mice with corneal alkali burn.

METHODS: Sixty BALB/c mice were divided into three groups(experimental group A, experimental group B and control group C), 20 mice in every group and their corneas in the right eyes were burned with alkali(1mol/L NaOH). The experimental group A received recombinant canstatin proteins drops with 3μg/mL. The experimental group B received recombinant canstatin proteins drops with 5μg/mL and the control group C was treated with physiologic saline. At different time points(1, 3, 7 and 14 d)after alkali burns, the mice were killed and the growth of epithelial defect and corneal neovascularization(CNV)were observed with an operation microscope. The expressions of MMP-2 and TIMP-2 in cornea were measured by the Western blot technique, and the results were analyzed by enhanced chemiluminescent(ECL).

RESULTS: The areas of epithelial defect and corneal neovasularization significantly reduced in mice treated with recombinant canstatin proteins compared to mice treated with physiologic saline at 3, 7 and 14d after alkali-induced injury( all P<0.01); the neovasularization was suppressed and the area of CNV was less than that in control group C(all P<0.01). Western blot analysis showed that the expression levels of MMP-2 in experimental group A and B were significantly lower than that in control group C(P<0.01)and the expressions of TIMP-2 in experimental group A and B were significantly higher(P<0.01); the level of MMP-2 in experimental group B were lower than that in experimental group A on day 14(P<0.05), while the level of TIMP-2 in experimental group B were significantly higher than that in experimental group A on day 7 and day 14(P<0.05).

CONCLUSION: Recombinant canstatin proteins may suppress the expression of MMP-2, upregulate the expression of TIMP-2 in cornea cells and the infiltrated inflammatory cells, lower the rapid resolution of cornea and ulceration, and play a vital role in the remodeling of alkali treated cornea in mice.