Objective It has been shown that pigment epitheliumderived factor (PEDF) is an effective anti-apoptosis agent on several kinds of cells of the central nervous system.This study aimed to evaluate the effect of PEDF on pressure induced retinal ischemia in a rat model. Methods Retinal ischemia was induced by increasing the intraocular pressure to 110 mm Hg for 45 minutes via an intracameral catheter.Ten microlit ers (0.1 mu;g/mu;l) PEDF was injected into the vitreous of 4 eyes of each group im mediately after reperfusion and 4 additional eyes received only normal saline as vehicle controls.The animals were euthanized at 2 or 7 days after reperfusion.T he effect of PEDF on retinal degeneration was assessed by measuring the thicknes s of the inner retinal layers (MTIRL) and counting the retinal ganglion cells (R GC) on plastic embedded retinal sections. Results The MTIRL and the RGC counting in eyes treated with intravitreal PEDF were significantly higher than those in vehicle controls (118.1plusmn;5.0) mu;m vs(94.9plusmn;3.0) mu;m (Plt;0.05);(6.0plusmn;1.0) cells/100 mu;m vs (4.5 plusmn;0.5) cells/100 mu;m (Plt;0.05) 7 days after reperfusion,respectively． Conclusion Intravitreal administration of PEDF can ameliorate an ischemiareperfusion retinal injury and may be useful to prevent neuronal degeneration in the inner retina. (Chin J Ocul Fundus Dis, 2001,17:138-140)
Objective To monitor the release of amino acids of the whole retina during and after experimental glaucoma by increasing the intraocular pressure （IOP）． Methods Experimental glaucoma was induced in one of the two eyes of rabbits by increasing IOP at 120 mm Hg for 45 min under infusion of saline in anterior chamber；then the pressure was released and the needle inserted into the anterior chamber was removed，this state was maintained for another 45 min．Every 15 min during the experiment 5 rabbits were killed and experimental eyes were enucleated．Aliquots（20 μl）of the retinal extracts（see below）were mixed with ophthaldialdehyde reagent and analysed for amino acid content by the HPLC method of Wangwei，using a 150 mm×4.6 mm,5 μm C18 column． Results A large increase in the release of glutamate，but not of the other three amino acids monitored，occurred during initial experimental ocular hypertension．It reached peak value of（111.73±17.46）10-5 mmol/g at 15 min of hypertension．15 min after release of intraocular pressure，again，immediately large and specific increase in the concentration of glutamate was reached to（102.96±51.91）10-5 mmol/g．In eyes subjected to paracentesis of anterior chamber，no difference was found between experimental eyes and controls. Conclusion These results suggest that glutamate is triggered by increasing the IOP，and it releases not only during the period of experimental ocular hypertension，but also afterwards. (Chin J Ocul Fundus Dis, 2002, 18: 146-148)
Objective To observe the affection of optic nerve under acute ocular hypertension and the effect of protection of bFGF on optic nerve. Methods BSS was perfused into anterior chamber of rabbits to increase the intraocular pressure to cause retinal ischemia. A computer image analysis system was used to count the optic nerve axons.Eyes were intravitreally injected with bFGF and then the number of optic nerve axons of the normal rabbits,and hypertension with and without bFGE treatment groups were counted respectively. Results The number of optic nerve axons in ocular hypertension eyes was less than the normal eyes(P=0.00003).The bFGF treated eyes had more optic nerve axons than the controls(P=0.0078). Conclusions The acute ocular hypertension may cause the loss of the nerve axons,and bFGF may be effective in protecting optic nerve in acute ocular hypertension. (Chin J Ocul Fundus Dis,2000,16:94-96)
Purpose To investigate whether experimental autoimmune uveitis can be induced equally in different rats by urea soluble fraction of bovine melanin-associated antigen(USF-BMAA),and,if so,difference among them. Methods Lewis rats,F344 rats,Wistar rats were immunized with USF-BMAA emulsified with complete Freud is adijuvant and Bordelella pertussis to induce experimental autoimmune uveitis.The animal models were investigated clinically and histopathologically and compared with each other. Rusults Experimental autoimmune uveitis could be induced in Lewis rats,F344 rats and Wistar rats with US-BMAA.Clinical and histopathalogical examination showed that bilateral ocular inflammation developed after immunization 9-13 days.Although inflammation was mainly located in anterior uvea,a mild focal choroiditis was noted in those with severe anterior inflammation.No inflammation was observed in the retina and pineal gland.Experimental autoimmune uveieis induced with USF-BMAA was similar to experimental autoimmune anterior uveitis incited with BMAA presented by other authors.Inflammation induced with USF-BMAA in F344 rats and in Lewis rats was quite similar in the severity and course of the model.But the inflammation was less in Wistar rats compared with that in Lewis rats and F344 rats. Conclusion Experimental autoimmune anterior uveitis was successfully induced with USF-BMAA in Lewis rats,F344 rats and Wistar rats.The difference with regard to the severity among these aminals were propably attributed to their genetic bankground. (Chin J Ocul Fundus Dis,1998,14:149-152)
Objective To observe the histological changes and apoptosis of retinal cells in pigmented rabbits treated by transpupillary thermotherapy (TTT) with different laser power. Methods Fourteen pigmented rabbits (28 eyes) were divided averagely into seven groups（control group, 50, 70, 90, 110, 130, and 150 mW group）according to different laser power of TTT. Light microscopy was performed to observe the histological changes, and TDT-mediated biotin-dUTP nick-end labeling (TUNEL) technique and flow cytometry (FCM) examination were used to detect the apoptotic cells 24 and 48 hours after photocoagulation, respectively. Results The color of retinal burn speckles changed from offwhite to white and super white with the diameter enlarged gradually as the laser power of TTT increased. The results of light microscopy revealed that compared with the control group, the retinal tissue did not change much in 50-70 mW group; in 90-130 mW group, the retinal structure was integrated, but the cone and rod cells became swollen and condensed nuclei and cytoplasmic vacuolization were seen in the inner nuclear layer. The difference of retinal structure in 50-130 mW group 24 and 48 hours after photocoagulation and control group was not significant. In 150 mW group, tumefaction and degeneration were observed in each layer of retina and the inner and outer segments of photoreceptor cells lost 24 hours after photocoagulation, and obvious necrosis and cell loss of retinal tissues were detected hours after photocoagulation. The results of TUNEL examination indicated that positive cells were found in outer nuclear layer in each photocoagulation group which increased as the laser power of TTT was enhanced; the apoptosis gradually involved the inner nuclear layer and ganglion cell layer. The results of flow cytometry (FCM) examination showed the peak of apoptotic cells in each photocoagulation group 24 hours after photocoagulation. Conclusion Under certain subthreshold photocoagulation (50-70 mW), retinal tissue of rabbits does not change much but apoptosis of photoreceptor cells increase significantly. As the laser power of TTT increases, the retinal tissues become swollen, degenerated and even necrotic; cellular apoptosis gradually involves the inner nuclear layer and ganglion cell layer. (Chin J Ocul Fundus Dis, 2006, 22:249-252)
Purpose To estabalish a quantifying model of retinal neovascularization suitable for the study of pathogenesis and therapeutic intervention for the retinal neovascularization． Methods Sixteen one-week-old C57BL/6 mice were exposed to 75% oxygen for 5 days and then to room air and 16 mice of the same age kept in room air as controls.Ink-perfused retinal flatmount was examined to assess the oxygen-induced changes of retinal vessels.The proliferated neovascular response was quantitated by counting the nuclei of endothelial cells of new vessels extending from the retina into the vitreous in 6 mu;m sagittal cross sections． VEGF and bFGF were determined on the cross-sections after immunohistochemcal stain. Results Constriction and closure of the blood vessels were found under the hyperoxia condition,and dilation and proliferation were found under the relatively hypoxia status.There was a mean of 24 neovascular nuclei per cross-section in the oxygen-treated retina and less than 1 nucleus in the control group (P＜0.001).VEGF stain was found ber in the inner retinal layer of oxygen-treated mouse than in that of the controls. Conclusion The quantifying model of retinal neovascularization may fascilitate the further researches of medical intervention and pathogenesis of retinal neovacularization. (Chin J Ocul Fundus Dis，2000，16：213-284)
Objective To investigate the effect of suppression of ischemia-induced retinal neovascularization by VEGF antisense oligodeoxyribonucleotides. Methods Mouse models of hyperoxia-induced ischemic retinopathy were established. Retrobulbar injections were performed with VEGF antisense oligodeoxyribonucleotides or NS in 4 groups:normal control and various doses respectively. The nuclei of new vessel buds extending from the retina into the vitreous in differ ent groups were counted and compared under the light microscope. Results There were plenty of new vessel buds in the eyes of mice in hyperoxic condition., while the number of the nuclei of new vessel buds is less in the murine eyes with retrobulbar injection of VEGF antisense oligodeoxyribonucleotides,especially the nuclei were redused with 59.3% in eyes with large dose. Conclusion The proliferation of retinal new vessel may be suppressed by using the retrobulbar injection of VEGF antisense oligodeoxyribonucleotides. (Chin J Ocul Fundus Dis, 2001,17:141-143)
PURPOSE:To measure the concentration changes of tumor necrosis factor a (TNF-alpha;)in vitreous during the development of experimental PVR induced by macrophages and explore the initial and mediated factors which stimulate the cellular proliferation. METHODS:Rabbit PVR model was induced by macrophages and the vitreous was taken at the 7th,14th,21st and 28th day and 4 eyes in each group. The TNF-alpha; levels in vivreous of the above examinated and control eyes were measured with an ELISA kit. RESULTS:The TNF-alpha; level in the vitreous reached its peak 434mu;g/ml at 21st day in the mod-el, then rappidly decreased to 122mu;g/ml at 28th day. CONCLUSION:The changes of TNF-a in the vitreous of the PVR model were parallel to the natrual phases of the development of PVR,indicating TNF-alpha; may play an important role in initiating and mediating the inflammation and cellular proliferation in the vitreous. （Chin J Ocul Fundus Dis,1997,13: 231-233）
Objective To observe the pathological and functional changes of retinal photochemical damages exposed to green flurescent light. Methods The Sprague Dawley rats were continually exposed to green fluorescent light with an illuminancem level of (1 900plusmn;106.9) Lx for 24 hours.The changes of retinal morphology and morphometrics and flash electroretinogram were studied before light exposure and at the 6th hour,6th day and 14th day after light exposure. Results At the 6th hours after light exposure,the outer nuclear layer(ONL)of retina becoma thinner compared with that bfore light exposure.The thickness of ONL decreased by 23.91% and the inner and outer segments appeared disorderly arranged.At the 6th day after light exposure the thickness of ONL is thinner than that at the6th hour,i.e.decreased by 46.6%. At the 14th day after light exposure the thickness of ONL decreased by 42.40%.Flash electroretinogram showed that the amplitudes of a and b wave decreased continuously at the 6th hour and 6th day and unrecovered at the 14th day after light exposure. Conclusion This model might be an ideal one for research on retinal photochemical damage. (Chin J Ocul Fundus Dis,1998,14:101-103)
Purpose To evaluate the prostag landins(PG) levels and to identify the effect of dexamethasone(DXM) on PG in response to photochemical insult in rat retina. Methods The experiments were performed on 36 SD rats which were separated into two groups,control and treated groups,and the latter received daily intraperitoneal injections of DXM (1 mg/kg) for 5 consecutive days,starting 3 days before light exposure.The animals were continually exposed to green fluorescent light(510-560 nm)with an illuminance level of (1900plusmn;106.9)lx for 24 hrs.The retinal concentration of PGE 2 and 6-keto-PGF1alpha; were tested at 6hrs,1,3,7 and 14 days after light exposure. Results The PGE2 and 6-keto-PGF1alpha; levels of the control groups (37.50plusmn;2.75,48.06plusmn;4.0 4,81.90plusmn;4.89) pg/mg and (4.68plusmn;0.69,7.50plusmn;0.57,10.40plusmn;0.71) pg/mg had significantly higher values than those of the treated rats(20.60plusmn;4.28,37.36plusmn; 3.34,54.85plusmn;4.57) pg/mg and (2.50plusmn;0.59,4．68plusmn;0.81,6.87plusmn;1.10)pg/mg (Plt;0.01) after 6 hrs,1 and 3 days light exposure respectively. Conclusion By inhibition of PG synthesis,the DXM may play an ameliorative effect on retinal photochemical injury of rats. (Chin J Ocul Fundus Dis,1999,15:94-96)