Basic Fibroblast Growth Factor (bfgf) On Rat Retinal Ischemia - Reperfusion Injury In The Treatment Of The Role Of Experimental Research

Objective To observe histologic and ultrastructure changes of the effects of recornbiant basic fibroblast growth factor(bFGF) on rat retina ischemia-reperfusion injury. At the same time investigate the effects of bFGF on the expression of bax and bcl-2 protein expression in retina after ischernia-reperftision injury. To discuss the therapeutical effect of bFGF and to provide theoretical basis for the pathogenesis and treatment of ischemia-reperfusion diseases. Methods 48 Wistar rats were divided into ten groups randomly. Raising intraocular pressure to induce retinal ischernia. One hour later remove the pressure and the blood stream returned normal. It lead to retinal ischemia-reperfusion injuiy Some rats were treated with bFGF. The retinal histological changes were observed by light microscope and electron microscope. In addition, with computer image analysis system, we measured the thickness of the inner retinal layer(IRL, between the internal limiting membrane and interface of the outer plexiform and the outer nuclear layer). To count the number of retinal ganglion cells (RGCs). The expression of bax and bcl-2 were determined by SABC (Stept Avidin-Biotin Complex) immune histochemistry. The positive stain sections were analysist by computer image analysis system. Results: 1. The retinal tissue structure is normal in the normal group. In the control group we can find edema of retinal(especially in the neuron fibrary layer and inner plexiform layer) in the early stage after ischemia-reperfusion injury, and the retinal atrophy, degeneration and necrosis were found in the later period. We can also found that the IRL became thinner and the RGCs was much less than normal group. In the treated group, the edema was much less than control group in the early 3 stage and the number of the RGCs were more than control group. 2. In the normal group, the expression of bax protein wasn't found. In the control group the expression can be found weakly 2 hours after ischemia-reperftision. Six hours the expression is clear, 24 hours at a peak, then decreased at 48 hours, but it still maintained a high level. It became almost the nomrnl level after 168 hours. In the treated group, the expression was very weak. It began to appear after 6 hours. The stainess is significant after 12 hours and the peak is also 24 hours. It almost disappeared at about 120 hours. The expression of bcl-2 changed little during the course. Conclusion 1. The main histologic changes of ischemia-reperfusion injury retinal induced by raising intraocullar pressure were a significant decrease in the thickness of the IRL and in the number of RGCs. 2. During the course of retinal ischernia-reperfusion injury, the expression of bax protein maintained a high level. It suggests that bax protein may affect the apoptosis of the retinal ganglion cells. 3. That bFGF can decrease the degree of the thinner of IRL and the loss of RGCs. 3. We found that bFGF has therpeutical effect on ischemia-reperfusion injury. It may be used in retinal ischemia-reperfusion injury diseases.