Objective Avascularity is the key feature of cornea.Corneal neovascularization would develop because of infection,surgical trauma,and some other reason.Acuity of vision would be seriously damaged.To investigate the effect of N-desulfated heparin on the expression of basic fibroblast growth factor(b-FGF)and transforming growth factor-betal(TGF-β1)in corneal neovascularization(CNV)of rats.The mechanism of neovascularization is multiplicity.Wilderness growth factors and regulatory factors participate this process.The purpose of this study was to detected the expression of b-FGF and TGF-β1 in the rat alkali burned corneal,This experiment is considering the effect of the N-desulfated heparin for alkali burn of the rat cornea to investigate the effective and approach the mechanism of action,and provide theoretical basis for effective treatment for cornea alkali burns.Methods Corneal neovascularization model was established by alkaline burning. Forty rats were randomly divided into four groups:â… group(twelve) the received 0.5g/L N-desulfated heparin 0.05ml injected under the conjunctiva.,â…¡group(twelve) was treated Dexmethason(0.5mg) injected under the conjuncti va,â…¢group the blank(twelve) control group was treated injected the normal salinc under the conjunctiva.,â…£group(four) the normal group.The growth of neovascularization was observed under slitlampmicros copy.The expression of b-FGF and TGF-β1 in CNV(cornealnevascularization)of each rat were detected by immunohistochemical staining.Result Theâ… group inhibit the growth of CNV significantly compared with theâ…¡control group.The growth total area of CNV(corneal-neovascularization ) inâ… group at various time points(ld,3d,7d,10d)was reduced significantly (P<0.05).Immunohistochemistry showed that the expression of b-FGF and TGF-β1 in experimental group was lower than that inâ…¡andâ…¢group.Conclusion bFGF and TGF-β1 are intimately correlated during the development of corneal neovascularization,and some dosage of N-desulfated heparin can decrease the expression of b-FGF and TGF-β1 to inhibit the occurrence of CNV.
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