The Expression Of PKC, P53 Protein And CyclinD1 In Rat Retina In Ischemia/Reperfusion Injury And After BFGF Treatment

[Objective] To investigate the action mechanism of basic f ibroblast growthfactor(bFGF) injected into the vitreous cavity on experimental retinalischemia/reperfusion injury, and provide theoretical basis to the therapeutical useof bFGF on retinal ischemia/reperfusion injury. (Methods] 28 rats were dividedinto normal (4 rats), ischemia (24 rats, left eye) and treatment group (24 rats, righteye) randomly; accord ing to the different time after reperfusion, the ischemia andtreatment group were further divided into In, 6h, 12h, 24h, 48h, and 72h subgroups (4rats/subgroup) . The rat model of experimental retina ischemia/reperfusion injurywas made by increasing the intraocular pressure. Then the rats were put to deathat 1st, 6th, 12th, 24th, 48th,and 72nd hour after intravitreous injection ofbFGF (treatment group) or balanced saline solution(ischemia group). The expressionsof protein kinase C( PKC),P53 protein and CyclinDl of different time courses weredetermined by strept-avidin-biotin complex(SABC) immunohistochemistry.(Results] 1. In ischemia group, there were PKC expressions at 6th hour afterreperfusion in the ganglion cell layer and nerve fiber layer, and the expressionsincreased as time courses prolonged;the expression reached the peak at 24th hourafter reperfusion, and PKC not only stongly expressed in the ganglion cell layerand nerve fiber layer, but also expressed a few in the inner nuclear layer; at 48thhour PKC expressed still strongly; at 72nd hour, the expression decreased alittle, but remained a fairly high level. 2. In ischemia group, there were P53 proteinexpressions at 6th hour after reperfusion in the ganglion cell layer and nerve fiberlayer, and the expressions increased as time courses prolonged;the expressionreached the peak at 24th hour after reperfusion, and P53 protein not only stonglyexpressed in the ganglion cell layer and nerve fiber layer, but also expressed afew in the inner nuclear layer; at 48th hour P53 protein expressed still strongly;at 72 nd hour, the expression decreased obviously.3. In ischemia group, there wereCyclinDl expressions at 6th hour after reperfusion in the ganglion cell layer andnerve fiber layer, and the expressions increased as time courses prolonged;theexpression reached the peak at 24th hour after reperfusion, and CyclinDl not only stongly expressed in the ganglion cell layer and nerve fiber layer, but also expressed a few in the inner nuclear layer; at 48th hour CyclinDl expressed still strongly; at 72 nd hour, the expression decreased obviously. 4. In treatment group, the change trend of PKC, P53, and CyclinDl expressions was similar except that the expression amount was relatively obviously less. There were statistical significance (P < 0.05) between the ischemia group and treatment group at 6th, 12th, 24th, 48th,and 72nd hour after reperfusion. [ Conclusions ] Retina ischemia/reperfusion injury can cause the increase of PKC, P53 protein and CyclinDl in retina ganglion cell layer, nerve fiber layer and inner nuclear layer; PKC, P53 protein and CyclinDl may be involved in the mechanisms of retina ischemia/reperfusion injury by playing parts in apoptosis; bFGF can inhibit the increase of PKC,P53 protein and CyclinDl in retina ischemia/reperfusion injury.Postgraduate Yuan Chunyan(Ophthalmology) Directed by Prof. Niu Yingjun...