The Effect Of Urokinase On Retinal Ganglion Cells Apoptosis Induced By Chronic Ocular Hypertension In Rats

BackgroundGlaucoma is the second cause of blindness in the world, is expected in2020, the world will have400million patients eventually blindness due to glaucoma. Death of retinal ganglion cells (Retinal GanglionCells, RGCs) in glaucoma is apoptosis. There are many medicines to protecte the RGCs, neuroprotection medicines are mainly concentrated in the research phase of the in vitro and in animal experiments, there are still a lot of problems. Our previous clinical study found that urokinase glaucoma can improve eyesight, improve vision. In this study, chronic ocular hypertension rat RGCs apoptosis process by observing the urokinase preliminary exploration of its possible neuroprotective mechanism.Methods30Sprague Dawley male rats were randomly assigned to three groups(normal control group, model group, Urokinase treatment group). The chronic ocular hypertention model of glaocoma was made by cauterizating the episcleral veins. The IOP of rats were measured by handheld tonometer(Tono-pen AVVI). Urokinase was given intraperitoneal injections to the Urokinase treatment group after IOP elevated continuously for7d, while the same amount of sodium chloride was given to the other two groups. The rats eyes were made into eyeball samples after4w. Eye sections were stained with hematoxylin and eosin. The apoptosis of RGCs is inspected bv TUNEL staining. The bcl-2expression was inspected by immunohistochemistry.ResultsThe mean postoperative IOPs were about40%higher than base IOPs and the conditions were maintained for4weeks. No TUNEL-positive cells were found in the normal control group. Signicantly more TUNEL stained cells were found in the model group(8.08±0.89) and TMP group(3.48±1.83). The TUNEL-positive cells in model group and Urokinase group was significant than that in the normal group(P<0.05). Bcl-2showed weak expression in the retina of the normal control group. Bcl-2protein expression were increased significantly in cauterized eyes compared with control eyes(P<0.05). However, the expression of bcl-2was up-regulated in Urokinase-treated group as compared with model group. There was significant difference (P<0.05).ConclusionsUrokinase may block apoptotic cell death in the GCL through upregulation of the expression of bcl-2.