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Objective To investigate the mechanisms of paeoniflorin in protection of retinal ischemia injury.Methods Fifty-four male specefic pathogen free (SPF) degree Wistar rats were randomly divided into normal control group,model control group and paeoniflorin group.Retinal ischemia injury was induced by raising the intraocular pressure of right eyes of rats to 110 mmHg for 30 minutes.The rats of paeoniflorin group were administrated through intraperitoneal injection of 5 mg/kg paeoniflorin each day for 14 days.OCT and electroretinogram (ERG) were performed to detect the thickness of retinal nerve fiber layer+retinal ganglion cell layer+inner plexiform layer (NGI)and electrophysiological changes of retina,respectively.Retrograde labelling of retinal ganglion cells (RGCs) was used to evaluate the survival number of RGCs.Western blot analysis was used to detect NLRP3,apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC),cleaved caspase 1 (c-caspase 1),IL-18,and IL-1β expression.The use and care of animals complied with the statement of the Association for Research in Vision and Ophthalmology (ARVO) and Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission.Results The thickness of retinal NGI in model control group was (58.2 ± 1.7) μm,which was significantly lower than (84.8 ± 1.9) μm in normal control group and (71.1 ±2.4) μm in paeoniflorin group (both at P＜0.05).The amplitudes of A and B waves in paeoniflorin group and normal control group were significantly higher than those in model control group (both at P＜0.05).The number of RGC in model control group was significantly lower than that in paeoniflorin group and normal control group (both at P＜0.05).The relative expressions of NLRP3,ASC,c-caspase 1,IL-18 and IL-1β in model control group were significantly higher than those in normal control group and paeoniflorin group (all at P＜0.05).Conclusions The paeoniflorin can prevent retinal ischemia induced injury of the retina through NLRP3 inflammasomes pathway,which provides a new treatment strategy for clinical therapy.
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Objective:To study the effects of resveratrol on the expressions of Caspase-3 and Bcl-2 in the retina tissue of the rats with retinal ischemia-reperfusion injury(RIRI),and to investigate the therapeutic effect of resveratrol on the RIRI and its mechanism.Methods:A total of 90 SD rats were randomly divided into sham operation group,model group and treatment group,30 rats in each group.The RIRI models were established by pressing the anterior chamber of the rats.The rats in model and treatment groups received ischemia-reperfusion for 1,6,12,24,and 48 h;the rats in treatment group were treated with micro-syringe intravitreal injection of 0.5 nmol·L-1of resveratrol 5 μL.The retinal tissue structure was observed by inverted microscope.The expression levels of Caspase-3 and Bcl-2 in retina tissue were detected by immunohistochemistry and Western blotting methods.Results:The retinal tissue edema of the rats in model group was found with vacuolar degeneration of the ganglion cells,and the arrangement of the cell layer was loose;the number of retinal ganglion cells was decreased,the boundary was blurred,and the nerve fiber layer thinned obviously.The degree of retinal tissue structure,the degree of injury and the degeneration of ganglion cells in treatment group were lighter than those in model group.The results of immunohistochemistry showed that the expressions of Caspase-3 and Bcl-2 in the retina tissue of the rats in treatment group were significantly increased compared with model group.The results of Western blotting method showed that the expression levels of Bcl-2 protein in the retina tissue of the rats in treatment group at different time points were increased compared with model group;and there were significant differences at 24 and 48 h(P<0.05);the expression levels of Caspase-3 protein in treatment group at different time points were lower than those in model group(P<0.05).Conclusion:Resveratrol can improve the retinal tissue structure of the RIRI rats,and its mechanism may be related to decreasing the expression level of Caspase-3 and increasing the expression level of Bcl-2 in the retinal tissue.
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Objective: To study the effects of resveratrol on the expressions of Caspase-3 and Bl-2 in the retina tissue of the rats with retinal ischemia-reperfusion injury (RIRI), and to investigate the therapeutic effect of resveratrol on the RIRI and its mechanism. Methods: A total of 90 SD rats were randomly divided into sham operation group, model group and treatment group, 30 rats in each group. The RIRI models were established by pressing the anterior chamber of the rats. The rats in model and treatment groups received ischemia-reperfusion for 1, 6, 12, 24, and 48 h; the rats in treatment group were treated with micro-syringe intravitreal injection of 0.5 nmol · L1 of resveratrol 5 μL. The retinal tissue structure was observed by inverted microscope. The expression levels of Caspase-3 and Bl-2 in retina tissue were detected by immunohistochemistry and Western blotting methods. Results: The retinal tissue edema of the rats in model group was found with vacuolar degeneration of the ganglion cells, and the arrangement of the cell layer was loose; the number of retinal ganglion cells was decreased, the boundary was blurred, and the nerve fiber layer thinned obviously. The degree of retinal tissue structure, the degree of injury and the degeneration of ganglion cells in treatment group were lighter than those in model group. The results of immunohistochemistry showed that the expressions of Caspase-3 and Bel-2 in the retina tissue of the rats in treatment group were significantly increased compared with model group. The results of Western blotting method showed that the expression levels of Bel-2 protein in the retina tissue of the rats in treatment group at different time points were increased compared with model group; and there were significant differences at 24 and 48 h (P<0.05); the expression levels of Caspase-3 protein in treatment group at different time points were lower than those in model group (P<0.05). Conclusion: Resveratrol can improve the retinal tissue structure of the RIRI rats, and its mechanism may be related to decreasing the expression level of Caspase-3 and increasing the expression level of Bcl-2 in the retinal tissue.
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Objective To investigate whether paraptosis and autophagy have an effect on acute retinal ischemia-reperfusion injury (RIRI) in an experimental rat model that recapitulates features of acute hypertensive glaucoma and to explore the possible underlying mechanisms.Methods A total of 30 adult male Sprague-Dawley rats were randomly divided into RIRI group and control group.The acute RIRI model was induced with normal saline in the right eye of rats from the RIRI group by anterior chamber perfusion,while the rats in the control group left untreated.On day 1,day 3,day 7,day 28 after RIRI model establishment,the changes in morphology of retinal ganglion cells (RGCs) were observed by transmission electron microscopy (TEM),and the expression of microtubule-associated protein 1 light chain 3 (LC3) was measured by immumofluorescence methods.Results When compared with the control group,the number of cytoplasmic vacuoles predominantly derived from the progressive swelling of mitochondria and/or endoplasmic reticulum (ER) in RGCs were increased in the RIRI group from day 1 to day 28 by TEM.And ultra-structural analyses showed the double-or multiple-membrane autophagosomes were markedly accumulated in the cytoplasm of RGCs following acute RIRI.The average number of autophagic vacuoles in the cytoplasm of RGCs was 0.79 per 50 μm2 in the control group,and the average number of autophagosomes reached to a maximum on day 7 after acute RIRI at 2.29 per 50 μm2,which was statistically significant compared with the control group (P ＜ 0.05).Compared to the control group,LC3 expression in the cytoplasm of RGCs was up-regulated on day 1 after acute RIRI,which sustained throughout the experimental period.The percentage of LC3 positive cells in the retinal ganglion cell layer was 15.90％ in the control group,and the data was 46.95％ and 52.30％ on day 1 and day 28 after RIRI,respectively,both which were statistically significant compared with the normal control group (both P ＜ 0.05).Conclusion Both paraptosis and autophagy participate in death of RGCs after acute RIRI.Programmed cell death in different cells,either coexistence of multiple-cell death form or a single-cell death form,participates in the pathogenesis of acute RIRI.
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Objective To investigate the mechanisms of paeoniflorin in protection of retinal ischemia injury. Methods Fifty.four male specefic pathogen free ( SPF) degree Wistar rats were randomly divided into normal control group,model control group and paeoniflorin group. Retinal ischemia injury was induced by raising the intraocular pressure of right eyes of rats to 110 mmHg for 30 minutes. The rats of paeoniflorin group were administrated through intraperitoneal injection of 5 mg/kg paeoniflorin each day for 14 days. OCT and electroretinogram ( ERG ) were performed to detect the thickness of retinal nerve fiber layer+retinal ganglion cell layer+inner plexiform layer ( NGI) and electrophysiological changes of retina, respectively. Retrograde labelling of retinal ganglion cells ( RGCs ) was used to evaluate the survival number of RGCs. Western blot analysis was used to detect NLRP3,apoptosis.associated speck.like protein containing a caspase activation and recruitment domain (ASC),cleaved caspase 1 (c.caspase 1), IL.18,and IL.1β expression. The use and care of animals complied with the statement of the Association for Research in Vision and Ophthalmology ( ARVO ) and Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission. Results The thickness of retinal NGI in model control group was ( 58. 2 ± 1. 7)μm, which was significantly lower than ( 84. 8 ± 1. 9)μm in normal control group and(71. 1±2. 4)μm in paeoniflorin group (both at P<0. 05). The amplitudes of A and B waves in paeoniflorin group and normal control group were significantly higher than those in model control group ( both at P<0. 05 ) . The number of RGC in model control group was significantly lower than that in paeoniflorin group and normal control group ( both at P<0. 05). The relative expressions of NLRP3,ASC,c.caspase 1,IL.18 and IL.1β in model control group were significantly higher than those in normal control group and paeoniflorin group (all at P<0. 05). Conclusions The paeoniflorin can prevent retinal ischemia induced injury of the retina through NLRP3 inflammasomes pathway,which provides a new treatment strategy for clinical therapy.
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AIM: To observe the effect of curcumin on the retinal structure and the expressions of interleukin-23 (IL-23) and interleukin-17(IL-17) in the rat retina after retinal ischemia-reperfusion injury (RIRI).METHODS:A total of 60 male Sprague-Dawley(SD) rats were randomly divided into normal control group(NCG),model group(MG),low-dose curcumin group (LDCG) and high-dose curcumin group (HDCG) (n=15 per group).RIRI was generated by anterior chamber perfusion of normal saline to the right eye.Rats in LDCG and HDCG received an intraperitoneal injection of 20mg/kg/d and 100mg/kg/d curcumin respectively,at 30min before RIRI and once daily after RIRI.Retinal structure and inflammation were evaluated after hematoxylin and eosin-stained (HE) staining.Western-blot and enzyme-linked immunosorbent assay (ELISA) were used to measure the level of IL-23 and IL-17 expressions after RIRI.RESULTS: The retinal structure of NCG was normal.Retinal edema,empty spaces or loosely packed cells and inflammatory cell infiltration were observed in MG and LDCG groups,whereas the morphological changes in HDCG group were improved as compared to MG and LDCG groups.Western-blot assay and ELISA showed that IL-23 and IL-17 expressions increased significantly after RIRI (vs NCG,P<0.01).Moreover,curcumin reduced IL-23 and IL-17 expressions significantly (vs MG,P<0.01).CONCLUSION: Curcumin can inhibit leukocytes infiltration and improve the retinal pathologic changes.Furthermore,curcumin can reduce retinal IL-23 and IL-17 expressions significantly in a dose-dependent manner.
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Objective To investigate the effects of N-acetylserotonin (N-AS) on the expression of active caspase-3,Bcl-2 and Bax in rat retinas induced by retinal ischemia-reperfusion injury (RIRI).Methods Adult male Sprague-Dawley rats were randomly divided into the normal control group (6 cases),RIRI group (30 cases) and NAS group (30 cases),RIRI models in NAS group were established after giving NAS,the groups were sub-divided into 6 hours,12 hours,24 hours,48 hours and 72 hours group based on the time of RIRI.Morphologic changes were evaluated by HE staining.The expression of active caspase-3,Bcl-2 and Bax protein in the retina of rats was detected by immunohistochemistry.Results HE staining showed that the retinal structure in the normal control group was clear,and the cells in each layer were tightly packed;Each layer of retina was edema in the RIRI group after 6 hours and 12 hours,the edema gradually alleviated after 24 hours,the ganglion cells decreased gradually,the distribution was in disorder,with the prolongation of time,the retinal ganglion cells were defected;drug group of as Compared with RIRI group,the cell edema in the NAS group at 6 hours and 12 hours were obvious reduced,the cells in 24 hours,48 hours,72 hours group arranged regularly,the loss number of ganglion cells were reduced.The number of active caspase-3 positive cells in RIRI group increased at 6 hours after peffusion,the number was (561.15 ±37.19) cell ·mm-2,and reached the high level at 24 hours,the number was (1522.61 ±84.36) cell · mm-2,and then decreased gradually.The number of active caspase-3 positive cells in NAS group was significantly lower than that in RIRI group,the difference was statistically significant (all P ＜ 0.05).The expression of Bcl-2 positive cells in RIRI group began to decrease after 6 hours,and decreased to a low level at 24 hours,and the number of Bcl-2 positive cells in NAS group was significantly higher than that in RIRI group at each time point,the differences were statistically significant (all P ＜ 0.05).There were almost no Bax positive cells in the retina of the control normal group,and the Bax positive cells were found to be higher of the RIRI group at the 6 hours after RIRI,and reached the higher level at 24 hours,and decreased at 48 hours.The Bax positive cells of NAS group were significantly less than those in the RIRI group at different time points,and the differences were statistically significant (all P ＜0.05).Conclusion NAS can promote the expression of Bcl-2 protein in rat retina after RIRI,inhibit the expression of Bax protein,decrease the expression of active caspase-3 protein,alleviate cell apoptosis,and have neuroprotective effects.
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PURPOSE: To report a rare case of traction retinal detachment and retinal ischemia in inactive Takayasu's arteritis at ophthalmologic clinic. CASE SUMMARY: A 23-year-old woman presented with a floater, photophobia, and visual loss in her right eye one week prior to visit. She had no other systemic disease, such as diabetes mellitus or hypertension, or previous ophthalmic abnormalities except for a tumor in the adrenal gland. We found bilateral retinal ischemia and traction retinal detachment in the right eye on fundus examination without iris neovascularization. Pars plana vitrectomy, traction removal, endolaser treatment, and intravitreal bevacizumab injection were performed. Steroid eye drops and steroid systemic administration relieved the inflammation. On carotid doppler sonography, we found severe stenosis and thickness of the inner layer in both carotid arteries. We diagnosed the patient with an inactive phase of Takayasu's arteritis, which was conclusively correlated with the clinical features. Vascular anastomosis surgery along with follow-up was proposed by both the cardiology and vascular surgery departments. CONCLUSIONS: When a young patient presents with traction retinal detachment and retinal ischemia, Takayasu's arteritis should be considered for differential diagnosis and a systemic work-up should be performed as soon as possible.
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Feminino , Humanos , Adulto Jovem , Glândulas Suprarrenais , Bevacizumab , Cardiologia , Artérias Carótidas , Constrição Patológica , Diabetes Mellitus , Diagnóstico Diferencial , Seguimentos , Hipertensão , Inflamação , Iris , Isquemia , Soluções Oftálmicas , Fotofobia , Descolamento Retiniano , Retinaldeído , Arterite de Takayasu , Tração , VitrectomiaRESUMO
Objective To study the protective effect and Bcl-2 expression of salvia miltiorrhiza pretreatment on retinal ischemia-reperfu-sion injury ( RIRI) . Methods One hundred and thirty two Wistar rats were randomly divided into the normal control group, the ischemia-reperfusion group and the salvia miltiorrhiza pretreatment group. The model of retinal ischemia-reperfusion injury was constructed by increas-ing the intraocular pressure. The ischemia-reperfusion and salvia miltiorrhiza pretreatment group were divided into five subgroups according to the different reperfusion time (6 h, 12 h, 24 h, 48 h and 72 h). Observe the histological changes in retina by HE staining. The SABC ( strept avidin-biotin complex) and Western-blot were used to measure changes of Bcl-2 protein levels in retinal. Results The positive ex-pression of Bcl-2 protein was weak in normal group. In the ischemia-reperfusion group and salvia miltiorrhiza pretreatment group, the expres-sion of Bcl-2 protein began to increase at 6 hours after reperfusion, reached the peak at 24 hours after reperfusion, began to decrease at 48 hours after reperfusion, and started to weaken at 72 hours after reperfusion. The variation tendency of the two groups were the same, however, the expression of Bcl-2 was significantly stronger in the salvia miltiorrhiza pretreatment group compared with ischemia-reperfusion group, and there was significant difference between the two groups (P<0. 01). Conclusion Salvia miltiorrhiza pretreatment can protect the retina by reducing retinal ganglion cells apoptosis in retinal ischemia-reperfusion injury. The mechanism may be achieved by regulating the expression of Bcl-2 protein.
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Purpose: To analyze the change in the concentration of intraocular cytokines (ICs) in patients with retinal vein occlusion (RVO) before and after intravitreal ranibizumab therapy (IVR), and to find the correlations of IC with clinical activity of RVO and efficiency of treatment. Materials and Methods: Forty‑four patients aged 46–79 years old (mean age: 60.7 ± 7.5 years old) with RVO and macular edema (18 patients – with central RVO, 26 – with branch RVO) treated with IVR were included into the study. The concentrations of 27 cytokines were simultaneously measured in aqueous humor by flow fluorometry using Bio‑Plex Pro Human Cytokine Panel, 27‑Plex (Bio‑Rad Laboratories, USA) at baseline and after the first IVR. Control group consisted of 20 age‑matched patients. Results: The levels of 11 cytokines (vascular endothelial growth factor [VEGF], receptor antagonist interleukin‑1, interleukin‑6 [IL‑6], IL‑8, IL‑9, IL‑10, IL‑12r70, IL‑13, IL‑15, monocyte chemotactic protein‑1 [MCP‑1], regulated on activation, normal T expressed and secreted) were significantly (P < 0.05) different compared to control and significantly (P < 0.05) changed after IVR both in central and branch RVO. The patients were divided into two groups: the first ‑“effective” and the second ‑ “partially effective” therapy. The second group characterized by the higher concentrations of VEGF, IL‑8, IL‑10, IL‑17, and MCP‑1 at baseline compared to the first group. Conclusion: The patients with RVO were characterized by the increased levels of VEGF and other pro‑ and anti‑inflammatory cytokines and chemokines. Aqueous concentration of cytokines were different in patients with central and branch RVO and significantly changed after IVR. Insufficient response to IVR was associated with activation of immune‑inflammatory processes.
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Anamnesis: a three years-old female Colombian Paso Fino equine presented visual impairment related to an anesthetic intervention with two alpha-2-adrenergic agents (xylazine 0.8 mg/kg + detomidine 10 ug/kg). Clinical and laboratory findings: ophthalmologic exam resulted in positive threat test with evidence of impaired obstacle circumvention due to failure in perception of distances and details of objects, resulting in unsteady gait and mount inability. The eye fundus presented horizontal bands on the nontapetal area and mild peripapillary edema. Scotopic electroretinogram (ERG) was performed under white light evidencing a decrease in amplitude and increase in A and B wave latencies for both eyes, compared with the reference. Hyperreflective tapetal zones and retinal folds are also observed. Leptospira tests were negative (Patoc: 1.25, Icterohaemorrhagiae: 1.25, Grippotyphosa: negative, Pomona: negative, Canicola: 1.50, Hardjo: 1.25, Ballum: negative, Bratislava: 1.25). Therapeutic approach: dexamethasone (0.2 mg/kg IM, for three days) and a vitamin supplement were prescribed. Conclusion: administration of two alpha2- adrenergic agonists may cause retinal ischemia with later development of retinal degeneration in horses.
Anamnesis: Equino hembra paso fino 36 meses de edad que presenta déficit visual relacionado a un evento anestésico con 2 agentes alfa-2-adrenérgicos (xilacina 0,8 mg/kg + detomidina 10 ug/kg). Hallazgos clínicos y de laboratorio: Al examen oftalmológico presenta prueba de amenaza positiva, al sorteo de obstáculos evidencia alteración en la percepción de distancias y detalle de objetos, resultando en una marcha insegura e imposibilidad de monta. El fondo de ojo se observan bandas horizontales en la zona no tapetal y leve edema peripapilar. Se realiza ERG bajo ambiente escotopico con luz blanca y se observa una disminución en la amplitud y aumento de latencias en ondas A y B de ambos ojos, comparado con la referencia. Posteriormente se visualizan zonas de hiperreflectividad tapetal y pliegues retínales. Se realizó prueba de Leptospira con resultado negativo: Patoc: 1.25, Icterohaemorrhagiae: 1.25, Grippotyphosa: negativo, Pomona: negativo, Canícola: 1.50, Hardjo: 1.25, Ballum: negativo, Bratislava: 1,25. Aproximación terapéutica: se formula dexametasona a razón de 0,2mg/kg IM durante 3 días y luego un suplemento vitamínico. Conclusión: La mezcla de dos agonistas alfa2-adrenérgicos puede causar un evento isquémico retinal con el posterior desarrollo de degeneración retiniana en caballos.
Anamnesis: Equino fêmea passo fino 36 meses de idade que apresenta déficit visual relacionado a um evento anestésico com 2 agentes alfa-2-adrenérgicos (xilacina 0.8 mg/kg detomidina 10 ug/kg). Achados clínicos e de laboratório: Ao exame oftalmológico apresenta prova de ameaça positiva, ao sorteio de obstáculos evidência alteração na percepção de distâncias e detalhe de objectos, resultando numa marcha insegura e impossibilidade de monta. As faixas horizontais de fundo de olho são observadas no nontapetal área e edema peripapilar suave. Escotópica ERG foram realizados sob luz branca ambiente e uma redução na amplitude e aumento latências ondas A e B de ambos os olhos, em comparação com a referência é observado. Posteriormente áreas do tapete hyperreflectivity e dobras de retina são exibidos. Teste de Leptospira foi realizada com resultado negativo: 1,25 Patoc Icterohaemorrhagiae 1,25 Grippotyphosa: negativo, Pomona: negativo, canicola: 1.50, Hardjo: 1,25, Nes: negativo, Bratislava 1,25. Therapeutic abordagem: dexametasona é formulado a 0,2 mg / kg IM por 3 dias e, em seguida, um suplemento vitamínico. Conclusão: A mistura de dois agonistas alfa-2-adrenérgicos pode causar evento isquêmico da retina com o posterior desenvolvimento da degeneração da retina em cavalos.
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Background Retinal ischemia-reperfusion (RIR) injury is a common pathologic change.Its mechanism has not been identified.Objective This study was to investigate the relationship of microRNA-181a (miR-181a) ,tumor necrosis factor-α (TNF-α) and retinal ganglial cells (RGCs) in RIR injury.Methods RIR models were induced in 68 rats,then the rats were randomly divided into control group and RIR groups,including 0hour group,24-hour group and 72-hour group by random number table.Predicted target gene TNF-α was chosen,according to M iRanda,Targetscan and miRBase databases.Immunofluorescent labeling, Western blot and quantitative real-time PCR were used to identify the expression levels of miR-181a,TNF-α and RGCs.Immunofluorescent labeling of RGCs in retinal flat mounts was analyzed for RGCs counts.Results Compared with the control group, RGCs densitiy was obviously decreased in 24-hour and 72-hour RIR groups (P＜0.001).The expression level of mir-181a significantly decreased with reperfusion time in the RIR groups (P＜0.05).Futhermore, the expression level of miR181a was positively correlated with RGCs numbers (r=0.995 ,P=0.005).TNF-α and miR-181a were mainly located in inner layers of retina.As opposed to the changes in RGCs numbers and miR-181a expression,TNF-α in 24-hour group was obviously higher than that of the 0-hour group, though there was no statistical significance in overall correlation analysis.Conclusions In RIR,miR-181a may be involved in regulating RGCs apoptosis.TNF-α may be a target gene of miR-181 a.Interventions within 24 hours after reperfusion might be critical.Further study of miR181 a may help to explore new molecular targets for neuroprotection treatment.
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?Retinal ischemia - reperfusion injury ( RlRl ) is a common clinical disease, and the producing mechanism is still in research. Experimental and clinical research in recent years have showed that the mechanism of RlRl and oxygen free radicals, gene regulation, calcium overload, inflammatory cytokines and other factors are closely related. ln this article, we summarized the current situation that the scholars at home and abroad study traditional Chinese medicine extract of prevention and treatment of RlRl.
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PURPOSE: To evaluate the long-term results of intravitreal bevacizumab injection for macular edema secondary to branch retinal vein occlusion (BRVO). METHODS: Fifty-six eyes with macular edema secondary to BRVO were treated with intravitreal bevacizumab injection. They were classified into two groups, one group that received three initial intravitreal bevacizumab loadings at monthly intervals and a second group that received only one initial injection. In the two groups, additive injection was performed at recurrence. The best corrected visual acuity (BCVA), central macular thickness (CMT) and retinal ischemic change was analyzed for more than 12 months postoperatively. RESULTS: After 12 months of follow-up, mean BCVA improved and mean CMT reduced significantly in both groups (p < 0.05). However, the range of BCVA improvement and CMT reduction was wider in the three-injection group than in the single-injection group. Fluorescein angiography revealed posterior retinal ischemic changes; bevacizumab didn't seem to aggravate the ischemic change. No drug-related ocular or systemic side effects were observed in the follow-up period after intravitreal bevacizumab treatment except subconjunctival hemorrhage and a mild increase of intraocular pressure. CONCLUSIONS: In patients with macular edema secondary to BRVO, intravitreal bevacizumab injection was a safe and effective treatment, and a more significant visual improvement and reduction of macular edema was achieved after three initial loadings rather than after a single injection.
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Humanos , Angiofluoresceinografia , Seguimentos , Hemorragia , Pressão Intraocular , Edema Macular , Recidiva , Oclusão da Veia Retiniana , Veia Retiniana , Retinaldeído , Acuidade Visual , BevacizumabRESUMO
Retinal ischemia is a common cause of blindness and visual impairment.Some eye diseases,such as glaucoma,retinal artery occlusion and diabetic retinopathy,are associated with retinal ischemia.It is very important to build an ideal animal model which can imitate human retinal ischemia disease for investigating the pathological mechanism and treatment of retinal ischemia.Rodent is a popular choice for retinal ischemia model due to its availability and the similarity to human retinal blood supply.To provide a supportive evidence of retinal ischemia research,some literature concerning rodent models is reviewed and various methods to build the model are summarized,such as elevated intraocular pressure,optic nerve ligation,ligation of vessels,photo-chemistry,endothelin-1 injection and middle cerebral artery occlusion intraluminal suture,etc.Here,the specific protocols,the pathological changes and molecular mechanism of each model are reviewed.
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Branch retinal artery occlusion (BRAO) and branch retinal vein occlusion (BRVO) rarely cause neovascular glaucoma (NVG). A 58-year-old woman with hypertension and type 2 diabetic mellitus complained of progressive visual loss in her right eye for the previous 3 months. At initial examination, visual acuity was 20 / 63 in the right eye. Angle neovascularization was observed and the intraocular pressure (IOP) was 30 mmHg in her right eye. Fundus examination and fluorescein angiography showed BRAO combined with BRVO. We immediately injected intravitreal and intracameral bevacizumab in her right eye. The next day, we performed scatter photocoagulation in the nonperfusion area. One month later, visual acuity was 20 / 20 in her right eye and the IOP was 17 mmHg with one topical antiglaucoma agent. The neovascularization had regressed completely. We report a case of unilateral NVG which was caused by BRAO with concomitant BRVO and advise close ophthalmic examination of the iris and angle in BRVO with BRAO.
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Feminino , Humanos , Pessoa de Meia-Idade , Diagnóstico Diferencial , Angiofluoresceinografia , Fundo de Olho , Glaucoma Neovascular/diagnóstico , Pressão Intraocular , Oclusão da Artéria Retiniana/complicações , Oclusão da Veia Retiniana/complicaçõesRESUMO
Glaucoma, a neurodegenerative disease, is currently being treated by modulation of one of its primary risk factors, the elevated intraocular pressure. Newer therapies that can provide direct neuroprotection to retinal ganglion cells are being extensively investigated. Tumor necrosis factor-α, a cytokine, has been recognized to play an important role in pro and antiapoptotic cellular events. In this paper we review the relevant literature to understand (1) The association of increased expression of tumor necrosis factor-α with glaucomatous neurodegeneraion, (2) Modulation of tumor necrosis factor-α expression by exposure to various risk factors of glaucoma, (3) Downstream cellular signaling mechanisms following interaction of tumor necrosis factor-α with its receptors and (4) Role of tumor necrosis factor-α as a possible target for therapeutic intervention in glaucoma. Literature was reviewed using PubMed search engine with relevant key words and a total of 82 English language papers published from 1990 to 2010 are included in this review.
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Apoptose , Citocinas/uso terapêutico , Apoptose/fisiologia , Citocinas/farmacocinética , Citocinas/fisiologia , Glaucoma/fisiologia , Humanos , Pressão Intraocular/efeitos dos fármacos , Degeneração Neural/fisiologia , PubMed/estatística & dados numéricos , Oclusão da Artéria Retiniana , Células Ganglionares da Retina/efeitos dos fármacos , Literatura de Revisão como Assunto , Fator de Necrose Tumoral alfa/farmacocinética , Fator de Necrose Tumoral alfa/fisiologiaRESUMO
Purpose: This study aims to investigate the levels of aqueous vascular endothelial growth factor (VEGF) in diabetic patient groups in comparison to normal subjects, and to correlate elevated VEGF with the severity of diabetic retinopathy (DR). Materials and Methods: Aqueous samples were obtained from 78 eyes of 74 patients undergoing intraocular surgery and they were examined by the enzyme-linked immunosorbent assay. Color photographs, optical coherence tomography scans, and fluorescein angiography were used to evaluate patients preoperatively. Results: A strong statistical correlation was found to exist between the level of aqueous VEGF and the severity of DR (P < 0.001), whereas, the VEGF levels in a control group and a diabetic group without DR were not significantly different (P = 0.985). Aqueous VEGF levels were significantly elevated in patients with proliferative DR (PDR) as compared to the control group (P < 0.001), to diabetic patients without retinopathy (NDR) (P < 0.001), and to diabetic patients with nonproliferative DR (NPDR) (P < 0.001). The aqueous VEGF levels were significantly higher in patients with active PDR than in those with quiescent PDR (P = 0.001). On the other hand, a statistically insignificant (P = 0.065) correlation was found between elevated aqueous VEGF and the presence of macular edema in the NPDR group. Conclusions: VEGF was elevated in the aqueous humor of patients with DR compared to that in normal eyes. The aqueous VEGF level had a strong correlation with the severity of retinopathy along with a statistically insignificant difference in macular edema.
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Idoso , Humor Aquoso/metabolismo , Retinopatia Diabética/metabolismo , Retinopatia Diabética/patologia , Retinopatia Diabética/fisiopatologia , Ensaio de Imunoadsorção Enzimática , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Índice de Gravidade de Doença , Fator A de Crescimento do Endotélio Vascular/metabolismoRESUMO
Background Recently,the study on the cause of optic nerve damage induced by glaucoma is of concern in ophthalmology.Some research showed that the immune system is associated with glaucoma-induced optic neuropathy.Acute ischemia-reperfusion is an ideal model of studying optic neuropathy.ObjectiveThe present study investigates the effect of T and B lymphocyte deficiency on the retinal neurocytes of mice with acute intraocular hypertension.Methods Sixteen SPF CB-17/Icr.Cg-Prkdc~(scid)Lyst~(bg)/CrlVR mice 6-8 week-old (severe combined immunodeficiency mouse,SCID) were used in this study and 16 age-matched SPF wild type (C57BL/6) mice served as controls.The ischemia-reperfusion injury models were induced in the right eyes of 10 SCID mice and 10 C57BL/6 mice through intra-anterior chamber infusion of balanced saline solution for 45minutes to increase the intraocular pressure to 104mmHg,and the left eyes served as model controls.The other 6 SCID mice and 6 C57BL/6 mice served as normal control group.10g/L (2μL) of FlouroGold was injected into the brains of the mice for the labeling of surviving retinal ganglion cells 21 days after ischemia-reperfusion.The thickness of retinal inner nuclear layer was measured by H&E staining under the fluorescent microscope 21 days after ischemic insult.The use of the animals followed the Standard of Association for Research in Vision and Ophthalmology.Results In normal control mice,the morphology of retinal ganglion cells (RGCs) and retinal structure were similar between SCID mice and C57BL/6 mice.The differences in the numbers of RGCs and retinal thickness were insignificant between the two types of mice(P＞0.05).In the experimental mice,the surviving RGCs were strikingly increased in SCID mice (91%±5%) compared with C57BL/6 mice(78%±5%)(P=0.003).The thickness of the retinal inner nuclear layer was obviously thinner in the model eyes (22.44±1.70μm) compared to model control eyes (31.06±3.75μm) in C57BL/6 mice(P=0.004),but no statistically significant difference was found between the model eyes and model control eyes in SCID mice (33.52±2.13μm vs 34.06±3.00μm) 21 days after ischemia-reperfusion injury(P＞0.05).Conclusion T and B lymphocytes deficient mice show a better tolerance to acute intraocular hypertension than the wild type C57BL/6 mice.
RESUMO
Objective To study the effect of Yiqimingmu pill on ATPase and LD of retinal ischemia rabbit, and probe into its mechanism. Methods Thirty-two Japanese large-ear white rabbits were divided into four groups, normal group (A group), model group (B group), comparison group (C group) and treated group (D group). Retinal ischemia was made in B, C and D group. After the treatment of one month, testing the correspondent indexes and studying with statistics. Results After the treatment of one month, in B and C group, the content of ATPse was lower, while the content of LD was higher compared with A group. Conclusion Yiqimingmu pill is reliable in the treatment of retinal ischemia, and superior to Buzhongyiqi wan.