Objective To explore the effect of oxygen inhalation on the retinae of newborn rats and its mechanism.Methods We mimicked the retinopathy of prematurity(ROP) by putting the newborn rats in high concentrated oxygen. One-day old rats were put into the oxygen box with the oxygen concentration of 80% for continuous 7 days; then in air condition for 7 days. The arterial blood oxygen pressure, retinal superoxide dismutase (SOD), and malondialdehyde (MDA) of the rats (1,2,4,7,8,9,11,14 days old) were examined. The diameter of retinal vessels′main branch and the coverage rate of peripheral vessels were measured in 7- and 14-day-old rats by ink perfusion. The retinal neovascularization of rats (8,9,11, 14 days old) were observed by HE staining. The rats of the same age fed in air condition were in the control group.Results The differential pressures of blood oxygen of rats (1,2,4,7 days old) in study group were significantly higher than those in the control group (P＜0.01), while the differential pressures of blood oxygen of rats (8,9,11,14 days old) in study group were lower than those in the control group (P＞0.05). The contents of SOD of the retinae in the rats ( 1,2,4,7,8 days old) were significantly lower than those in the control group(P＜0.01, P＜0.05 ), while the contents of MDA were significantly higher than those in the control group (P＜0.01,P＜0.05). The diameter of retinal vessels′main branch in 7-day rats was 75% of the control group, and the coverage rate of peripheral vessels was 22% of the control group; and was 61% and 73% respectively in 14-day-old rats. The neovascularization could be seen in 16.7% of the rats in the study group and nought in the control group.Conclusion The damage of free radical of the retina in high concentrated oxygen and hypoxia situation after oxygen supply may be one of the most important mechanism of ROP. (Chin J Ocul Fundus Dis，2003，19：269-332)
Purpose To investigate nucleoside diphosphate kinase (NDPK ) expression of tumor metastasis suppressor gene nm23 in heterotransplanted model of retinoblastoma(RB) in nude mice，and analyse the correlation between the expression of nm23 gene and the formation and progression of heterotran splanted RB． Methods SP immunohistochemical method was used to detect the expression of nm23 gene product NDPK in 20 tumors of heter otransplanted RB model and normal retinal tissue． Results The negative staining of nm23/ NDPK was found in normal retinal tissue , whereas 100% expression rate in RB tumors with positive number of 48.73plusmn;2.37． No statistical significance of the expression of nm23/ NDPK was observed between the intraocular growth phase （I～Ⅲ grade） and invasive phase （ Ⅳ～Ⅴ grade）in heterotransplantedRB tumors． Conclusion The function of nm23 gene as a tumor metastasis suppressor in heterotra nsplanted RB tumors was less prominent ,but it may play a role in carcinogen esis and progrssion of RB and may predict poor prognosis． (Chin J Ocul Fundus Dis, 2001.17:47-49)
Objective To investigate the alteration of protein kinase C (PKC) and endothelin system in early diabetic rats, and the effect of specific PKC inhibitor on the expression of retinal endothelin-1 (ET-1). Methods The rats model with streptozotocin(STZ)-induced diabetes were set up. The expression of retinal PKC was detected by enzyme-linked immunoabsorbent assay (ELISA). The expression of retinal ET-1, ET-3, ET-A and ET-B receptor mRNA was determined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The alteration of retinal ET-1 mRNA after intravitreal injection of PKC inhibitor GF109203X in diabetic rats was also observed. Results The activities of membranous PKC were significantly increased in 2-week diabetic rats compared with that in normal rats（t=3.296 , P=0.008）, while activities of cytosolic PKC were unchangeable（t=0.138, P=0.894）. The expression of retinal ET-1 mRNA was significantly increased（P=0.008）, while no change was found in expression of ET-3, ET-A and ET-B mRNA（P=0.918，P=0.889，P=0.500）. After intravitreal in jection of 10-5、10-6、10-7 mol/L PKC inhibitor GF109203X in diabetic rats, the expression of retinal ET-1 mRNA was decreased in a dose-dependent manner compared with the control rats. Conclusion Activation of PKC and increased expression of ET-1 could be found in the retina of early diabetic rats, and PKC inhibitor could inhibit the expression of retinal ET-1. (Chin J Ocul Fundus Dis，2004，20：168-171)
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)
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)
Objective To investigate the damage to the retinal cells and apoptosis of retinal cells of rats after ischemia-reperfusion insult. Methods The retinal ischemia-reperfusion model was developed by increasing intraocular pressure to 109725 mm Hg in rat eyes. Morphological changes of the rat eyes were observed by means of routine histopathology with HE staining. Apoptosis of the retina was assayed by both DNA fragmentation gel-electrophoresis and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labelling (TUNEL). Results Compared with the normal control, no histopathological changes were revealed in the rat retinas 30 min after the ischemia and then reperfued for 24 h or 48 h. Retinal ganglion cell layer (RGL) and inner plaxiform layer (IPL) of the retina were observed, however, to become significantly thinner 60 min after the ischemia and then reperfued for 24 h or 48 h. Together with the pathological changes DNA ladder pattern was detected in the same group of the rats. Further, immunochemical stain of the eye demonstrated that TUNEL positive cells were localized in RGL and IPL of the retina. Conclusion Ischemia-reperfusion insult of the eye may remarkably damage the retina of the rat eye. The damage to the retinal cells is mainly localized within RGL and IPL and apoptosis is the important mechanism of the retinal disorder. (Chin J Ocul Fundus Dis, 2002, 18: 296-298)
Objective To investigate the expression and significance of inducible co-stimulator (ICOS) in experimental autoimmune uveoretinitis (EAU). Methods EAU was induced in 24 Lewis rats (immune group) by immunization with retinal S-antigen (50 mu;g) and complete Freundprime;s adjuvant, and another 4 rats were in the control group. Anterior segment of the ratsprime; eyes were observed by split microscope every day. Immunohistochemical staining was performed using polyclonal antibodies to ICOS on the sections of the spleen which were obtained from the rats in immune group at the 7th, 12th, 15th and 21st days after immunisation respectively. Western blotting was performed to investigate the dynamic expression of ICOS protein in the spleen. The same procedures were made at the corresponding time points in the rats in control group. Results A few ICOS positive cells were observed in the normal spleen. The number of ICOS positive cells in immune group increased obviously at the 7th and 12th days after immunization, reached the peak at the 15th day, and decreased at the 21st day which was still higher than that in the control group. The result of Western blotting showed that the dynamic changes of ICOS protein was identical with the changes of positive-cell number detected by immunohistochemistry. Conclusions The enhanced expression of ICOS happens before EAU occurs, which increases when the inflammation occurs and deteriorates, and decreases at the alleviative stage of EAU. It suggests that ICOS participates in the formation, development and disappearance of EAU and plays an important role in the incidence of EAU. (Chin J Ocul Fundus Dis, 2005,21:114-117)
ObjectiveTo observe the expression of connective tissue growth factor (CTGF) in injured model of retinal pigment epithelial (RPE) cells and the promoting effect of CTGF on migration of RPE cells.MethodsCultured monolayer-confluent human RPE cells were scraped with a trephine and a cotton stick, and set up the injured model of RPE cells with round scraped area. Immunohistochemistry and in situ hybridization(ISH) were used to detect the expression of CTGF protein and mRNA in injured RPE cells at distinct time points after injury. The number of RPE cells migrated to injured area was measured and the effect of CTGF on migration of RPE cells and the effect of dexamethasone (DEX) on the promoting process of CTGF were observed.ResultsThe results of immunohstochemistry and ISH indicated the weak positive expression of CTGF in RPE cells at the edge of scrape 6 hours after injury, and the positive expression increased gradually as time goes by after the injury. Strong positive expression of CTGF in RPE cells at the edge of scrape was found 24 and 48 hours after injury. Rebuilt human CTGF stimulated migration of RPE cells in a dose-depended manner, and DEX significantly inhabited the migration.ConclusionCTGF involves in the procedure of repair of injury of RPE cells, which may play an important role in the pathogenesis of intraocular proliferative diseases such as proliferative vitreoretinaopathy.(Chin J Ocul Fundus Dis, 2005,21:306-309)