Effect of KH902 in Inhibiting Suture Induced Corneal Neovascularization

YANG Ying-ying, ZHANG Ling, FU Ping.et al

Abstract

To evaluate the effect of topical KH902 on experimental corneal neovascularization (CNV) in rats. Methods Suture models of CNV were established in 60 adult healthy rats. The rats were randomly divided into 3 groups: Group A (20 rats) were treated with KH902 (KH902 30 mg/mL was injected subconjunctivally once every other day); Group B (20 rats) were treated with dexamethasone (0.1% dexamethasone was injected subconjunctivally once every other day); Group C (20 rats) served as blank control. CNV growth were observed by slitlamp microscopy 3, 7 and 14 d after suture. Medicines were administered 14 d after operations. CNV changes were observed and recorded 1, 7, 14, and 21 d after administration of medicines. VEGF expression in cornea was measured by immunohistochemistry. Results No significant differences were found in average areas of CNV between groups at 1 and 7 d after administration of medicines. At 14 and 21 d after administration of medicines, significant differences in average areas of CNV were found between Group A and Group C, and between Group B and Group C (P<0.01). Maximum expression of VEGF in corneal stroma was observed 14 d after corneal suture. The expression of VEGF decreased with medications, which was associated with neovascularization. Conclusion Topical use of KH902 inhibits corneal suture-induced CNV in rats without significant adverse corneal effect on eyes.

 

Keywords: KH902, Corneal neovascularization Suture Inhibition 

 

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References


Sen S, Takahashi R, Rani S, et al. Expression of differentially phosphorylated Rb and mutant p53 proteins in myeloid leukemia cell lines. Leukemia Res. 1993; 17(8) :639-647.

Donato NJ, Wu JY, Zhang L, et al. Down-regulation of interleukin-3, granulocyte-macrophage colony-stimulating factor receptor beta-chain in BCR-ABL ( + ) human leukemic cells; association with loss of cytokine-mediated Stat-5 activation and protection from apoptosis after BCR-ABL inhibition. Blood, 2001;9 7(9);2846-2853.

Druker BJ, Sawyers CL, Kantarjian H, et al. Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome. N Engl J Med, 2001;344(14);1038-1042.

Korsmeyer SJ. Shutter JR. Veis DJ. et al. Bcl-2/Bax, a rheostat that regulates an anti-oxidant pathway and cell death. Semin Cancer Biol, 1993; 4 (6); 327-332.

Korsmeyer SJ. Bcl-2 gene family and the regulation of pro-grammed cell death. Cancer Res, 1999; 59 ( 7 Suppl); 1693s- 1700s.

Li X, Alafuzoff I. Soninen H, et al. Levels of mTOR and its down stream targets 4ЕВР1» eEF2. and eEF2 kinase in relationships with tau in Alzheimer’s disease brain. FEBS J,2005;272(16):4211-4220.


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