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·AlM:To evaluate the visual and anatomic outcomes of intravitreal ranibizu mab injections for myopic choroidal neovascular ization ( mCNV) in Chinese patient s. ·METHOD S: This study is ar etrospective case.Thri ty-five p atients treated for mC NV were included in this study.Their eyes were treated with a single intravitreal injection of 0.5 mg ranibizumab following a pro re nata ( PRN) regimen indicated by persistent or recurrent CNV. Best correc te d visual acuity ( BCVA ) , CNV findings on fundus fluorescen t angio graphy ( FFA ) , central retinal thickness ( CRT ) on optical coherence tomography ( OCT ) , total number of treatments, and complications were evaluated. · RESULTS:The mean follow-up duration was 20mo (range 16-24mo).Twenty-eight patients (80%) were followed up for more 22mo.The mean baseline BCVA was 0.74 logarithm of the minimum angle of resolution (logMAR) [standard deviation (SD) 0.23] and improved significantly to 0.49 logMAR ( SD 0.31 ) ( P · CONCLUSlON:The long-term outcomes observed in this study suggest that intravitreal ranibizumab is safe and effective for treating mCNV.
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·AIM: To detect the effect of CTGF on the apoptosis in the diabetic retina with small interfering RNAs (siRNA) targeting with CTGF. ·METHODS: A total of 60 rats were divided into six groups including control group, diabetic 4,8,12,16 weeks group, and interference group. Diabetic rats were induced by STZ intra-peritoneal. At 4, 8, 12, 16 weeks after diabetic setting up, retinas were obtained from control, diabetic rats and diabetic animals treated by intravitreal injection of CTGFsiRNA to suppress the expression of CTGF mRNA. Retinal cells apoptosis was detected by Tunnel staining and mRNA expression of CTGF was analyzed by RT-PCR.·RESULTS: The levels of CTGF and the apoptosis in the retinas of diabetic rats were significantly higher than those in the controls. Apoptosis occurred at 4 weeks after a diabetic model setting up, became serious with the diabetes developing, while CTGF elevated at 8 weeks. The cell apoptosis counts increased to 25.8cells/mm2 at 24 weeks of diabetes. SiRNA-mediated inhibition of CTGF mRNA resulted in a significant decrease in apoptosis. Significant correlations were found between CTGF and apoptosis in the retina.·CONCLUSION: These results suggest that CTGF might be involved in retinal cells apoptosis which is a characteristic of early diabetic retina. siRNA targeting CTGF seems to have the advantage of ameliorating retinal cells lost.
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<p><b>BACKGROUND</b>Optic nerve injury, caused by retinal and optic nerve diseases, can eventually result in vision loss. To date, few effective treatments have been discovered to restore visual function. Previous studies showed that recombinant human erythropoietin (rhEPO) has a neuroprotective effect on the central nervous system, particularly in nerve injury. In this study, we investigated the effects of rhEPO on axonal regeneration and functional restoration following optic nerve injury. This was done by measuring the expression of growth associated protein 43 (GAP-43), a marker for neuronal regeneration, on the retina and flash-visual evoked potential (F-VEP).</p><p><b>METHODS</b>Adult Wistar rats were randomly assigned to rhEPO and control (saline) groups. Optic nerve crush injury models were established and rhEPO or saline were immediately injected into the vitreous cavity. The expression of GAP-43 was detected by immunohistochemistry and the F-VEP was measured pre-injury, immediately after injury, 1 week and 2 weeks post-injury.</p><p><b>RESULTS</b>No detectable staining for GAP-43 was observed in normal retina. In the control group, the level of GAP-43 expression was higher at 1 week post-injury, but decreased at 2 weeks. In the rhEPO group, the level of GAP-43 expression was notably higher at both 1 week and 2 weeks. At each time point post-injury, the expression of GAP-43 in rhEPO group was significantly higher than the control group (P < 0.05). Obvious changes in F-VEP examination were detected immediately after optic nerve injury, including significantly prolonged latency and decreased amplitude of the P1 wave. In the control group, the changes were still obvious at 1 week. The latency was decreased and the amplitude had slightly recovered to 28.23% of the normal value at 2 weeks. In rhEPO group, there was significantly more recovery than the control group at 1 week and 2 weeks post-injury (P < 0.05). The latency most close to the normal level and the amplitude had recovered to 65.51% of the normal value at 2 weeks.</p><p><b>CONCLUSIONS</b>rhEPO can prolong the expression of GAP-43 and increase its intensity after optic nerve injury, thereby promoting neural repair and axonal regeneration. Under the protection of rhEPO, the conduction velocity of the optic nerve recovered significantly. Therefore, rhEPO has neuroprotective effects on the optic nerve and promotes functional restoration of the optic nerve.</p>
Subject(s)
Animals , Humans , Rats , Erythropoietin , Pharmacology , Therapeutic Uses , Evoked Potentials, Visual , GAP-43 Protein , Metabolism , Immunohistochemistry , Neuroprotective Agents , Pharmacology , Therapeutic Uses , Optic Nerve , Optic Nerve Injuries , Drug Therapy , Random Allocation , Rats, Wistar , Recombinant Proteins , Retina , MetabolismABSTRACT
AIM:Investigating the expression of HIF-1α,apoptosis of retinal cells and the role of HIF-1α in apoptosis in rats' retinal ischemia-reperfusion injury.METHODS:The rat model of experimental retinal ischemia-reperfusion injury was established by increasing the intraocular pressure to 110mmHg(1kPa=7.5mmHg)in rat eyes.At different time points of post ischemia,the expression of HIF-1α of the retina was detected by immunohistochemicalstaining,and apoptosis of the retinal cell was detected by terminal deoxynudeotidyl transferase medialed deoxyuridine triphosphatebiotin nick end labeling(TUNEL).RESULTS:HIF-1α appeared in the cells of retinal ganglion layer and inner nuclear layer at 2 hours after ischemia.The expression reached to a peak,12 hours after retinal ischemia-reperfusion,then the expression was dedined.The apoptotiC Cells were mainly in inner nuclear layer and could be detected at the 12th, 24th and 48th hour after ischemia,the peak value was the group of 24th hour.CONCLUSION:Expression of HIF-1α in the rats' retina is greatly enhanced after ischemia-reperfusion,which may be involved in the retinal injury:the injury of retinal neurons Occurs partly in the form of apoptosis.The expression of HIF-1α may play an important role in cell apoptosis.
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AIM: To investigate the expression of vascular endothelial growth factor receptor 2 (VEGFR-2, also known as FLK-1) in laser-induced choroidal neovascularization (CNV) in mouse.METHODS: CNV was induced in C57BL/6 mouse eyes by krypton laser photocoagulation. Choroidal fiuorescein angiography and histopathological examination were used to assess the development of experimental CNV. Cryostat sections from lesions on day 10 after laser treatment and normal eyes were prepared for Immunohistochemistry for FLK-1.RESULTS: Laser-induced CNV developed in all lesions on day 10. The expression of FLK-1 was detected in endothelial cells, retinal pigmented epithelium (RPE)-like cells and fibroblast-like cells in neovascular lesions. In normal adult mouse retinas, FLK-1 expression was mainly observed in RPE cells, inner nuclear and ganglion cell layers.CONCLUSION: Our findings demonstrated that expression of FLK-1 may play a role in the formation of laser-induced CNV in mice, which suggest that FLK-L may be a promising potential target for antiangiogenesis therapy for CNV.
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· AIM: To investigate the possibility of FLK-1 as a therapeutic agent for choroidal neovascularization (CNV) in mouse by FLK1 monoclonal antibody.· METHODS: CNV was induced in C57BL/6 mouse eyes by krypton laser photocoagulation. Preoperatively and on the 3rd, 6th and 9th day after photocoagulation, the animals were intraperitoneally injected with 500μg FLK1 monoclonal antibody. Choroidal fluorescein angiography and histopathological examination were used to assess the development of experimental CNV quantitatively 10 days after laser treatment.· RESULTS: Laser-induced CNV developed in all lesions on the 10th day after the operation. The development of CNV was significantly inhibited in experimental group, indicated by choroidal fluorescein angiography and histopathological examination (P＜0.001).· CONCLUSION: Our findings suggest that FLK-1 may be a promising agent for anti-angiogenesis therapy for CNV.
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· AIM: To observe the inhibitory effect of triamcinolone acetonide (TA) on the proliferation of monkey choroidretinal endothelial cells (RF/6A) in hypoxia or normal conditions.retinal endothelial cells of rhesus monkey (RF/6A). The effect of TA on the cellular activity was observed by MTT,the effect on cellular proliferation and apoptosis was detected by flow cytometry (FCM).cycle were reduced and the proportion of cells in G2-M phase was increased under the hypoxia condition .TA had a great effect on the cell cycle of choroid-retinal endothelial cells of rhesus monkey and it induced apoptosis of endothelial cells. It relatively increased the S-phase cells and reduced G2-M phase cells under both normal and hypoxia conditions, which indicates its role in blocking cell cycle from s-phase to G2-M phase and reducing mitosis.RF/6A cells while TA has the opposite effect in both normal and hypoxia conditions. TA can also induce apoptosis of endothelial cells.