Objective To investigate the effect of proanthocyanidins (PC) on retina of rats with acute ocular hypertension. Methods The SpraqueDawley (SD) rats were randomly divided into the normal group, the model group and PC high or lowdosage group. The PC high or low dose group received 300mg/kg.d or 100mg/kg.d of PC in suspension solution for 5 days respectively. The normal group and the model group fed with distilled water for 5 days. Then acute ocular hypertension was induced in the model group and all PC groups, and after 48h of ocular hypertension the eyeballs were analyzed by electron microscope and UV spectrophotometer to measure the levels of superoxide dismutase(SOD), malonaldehyde (MDA), nitrogen monoxidum (NO), glutamic acid (Glu) and calcium ion(Ca2+). Results PC could raise the activity of SOD and reduced the levels of MDA,NO,Glu and Ca2+ in retina tissue. Electron microscope examination revealed that PC reduced retinal edema and ganglion cell apoptosis. PC also enhanced the SOD activity and suppressed the levels of MDA, NO, Glu and Ca2+. Conclusions PC can protect retina from acute ocular hypertension. The main mechanism might relate to anti-free radical oxidation, antagonizing calcium overloading, reducing toxicity of NO and Glu on the retina.
ObjectiveTo investigate the effect of erigeron breviscapus (EBHM) on ocular hypertension and the protective effect of retinal ganglion cells (RGCs) in rats by regulating mitogen activated protein kinase (MAPK) signaling pathway.MethodsSixty male Sprague-Dawley rats were divided into control group, model group, low-dose EBHM group (group A), medium-dose EBHM group (group B), and high-dose EBHM group (group C) by random number table method. There were 12 rats in the group, the left eye was used as the experimental eye. The rats of model group, group A, group B, and group C were infused with normal saline through the anterior chamber to construct an acute ocular hypertension model; the control group was given general anesthesia only. Then, 2-30 days after modeling, rats in the control group and model group were given 3 ml of normal saline once a day; rats in group A, group B, and group C were given 0.30, 0.45, and 0.60 g/100 g EBHM by intragastric administration, respectively, 1 time/d. The rat intraocular pressure was measured before modeling and 1, 14, and 30 days after modeling, and the proportion of high intraocular pressure model was measured. Thirty days after modeling, hematoxylin-eosin (HE) staining was used to observe the pathological changes of retinal tissue; immunofluorescence staining was used to detect the changes in the number of RGCs; real-time fluorescent quantitative polymerase chain reaction (RT-qPCR) was used to detect p38 in the retinas of rats in each group. The relative expression of MAPK and Caspase-3 mRNA; western blot was used to detect p38MAPK and phosphorylation in the retina of rats in each group relative expression of phosphorylate-p38MAPK (p-p38MAPK) and Caspase-3 protein. One-way analysis of variance was used for multi-sample comparison, and SNK-q test was used for comparison between two samples.ResultsOne day after modeling, none of the rats in the control group developed acute ocular hypertension, and the other groups were successfully modeled. Compared with the model group, the rates of acute ocular hypertension at 14 days after modeling in groups B and C were lower (χ2=98.701, P＜0.05), and the rates of acute ocular hypertension at 30 days after modeling in groups A, B, and C were 0. There was no statistically significant difference in the rates of acute ocular hypertension between 14 and 30 days after modeling in the A, B, and C groups (P＞0.05). The results of HE staining showed that the structure of the retina in the control group was complete, and the layers were clearly visible; the RGCs count was not abnormal, and the morphology was plump and round. The retina of rats in the model group became thinner; the number of RGCs was greatly reduced, the morphology was vacuolated, and the arrangement was sparse. The retina of rats in groups A, B, and C became thicker, and the number of RGCs increased, and the retina structure in group C was better restored. The results of immunofluorescence staining showed that the RGCs counts of rats in groups A, B, and C were higher than those in the model group, and the difference was statistically significant (F=297.514, P＜0.05); pairwise comparison between groups, group A was lower than that of group B and C Group (q=2.842, 5.263), group B was lower than group C (q=2.457), the difference was statistically significant (P＜0.05). The results of RT-qPCR and Western blot showed that compared with the model group, the relative expression of Caspase-3 mRNA (F=267.912) and protein (F=692.279) and the relative expression of p-p38MAPK protein in the retina of rats in groups A, B and C. The expression level (F=150.061) all decreased, and the difference was statistically significant (P＜0.05); pairwise comparisons between groups showed that Caspase-3 mRNA (q=6.977, 15.642) and protein (q=6.997, 15.642) relative expression levels and p-p38MAPK protein (q=12.443, 24.358) relative expression levels are lower than groups A and B, group B was lower than group A (q=11.678, 12.471, 10.204), the difference was statistical academic significance (P＜0.05).ConclusionsEBHM can significantly reduce intraocular pressure in rats with acute ocular hypertension, increase RGCs counts, and reduce retinal damage. Its regulatory mechanism may be related to the MAPK pathway.
Objective To observe and analyze the risk factors of secondary intraocular hypertension in diabetic macular edema (DME) patients after treatment with dexamethasone vitreous cavity implant (DEX). MethodsA retrospective observational study. A total of 352 patients with type 2 diabetes mellitus (T2DM) secondary macular edema diagnosed by ophthalmic examination and treated with DEX in Department of Ophthalmology of Harbin 242 Hospital from January 2016 to March 2022 were included in the study. Among them, 221 were males and 131 were females, with the mean age of (55.56±8.09) years. There were 194 patients with disseminated macular edema, 158 patients with cystoid macular edema. All patients underwent vitreous cavity implantation of DEX. Intraocular pressure (IOP) was measured once a month for 3 months after treatment, with IOP over than 25 mm Hg (1 mm Hg=0.133 kPa) or higher than 10 mm Hg from baseline as secondary intraocular hypertension. The relevant clinical data were collected, and the risk factors of secondary intraocular hypertension in DME patients after DEX treatment were analyzed by binary logistic regression. ResultsAmong 352 patients, 116 patients (32.95%, 116/352) were in the intraocular hypertension. Among them, 29 patients (25.00%, 29/116), 69 patients (59.48%, 69/116) and 18 patients (15.52%, 18/116) occurred intraocular hypertension at 1, 2 and 3 months after treatment, respectively. Compared with the normal IOP group, the IOP in the intraocular hypertension group increased significantly at 1, 2 and 3 months after treatment, with statistical significance (t=10.771, 21.116, 13.761; P＜0.001). Compared with normal IOP group, the patients in the intraocular hypertension group had younger age (t=6.967), longer duration of diabetes (t=5.950), longer axial length (AL) (t=14.989), higher proportion of DME grade 3 (Z=6.284), higher proportion of DEX implantation in pars plana (χ2=23.275), and higher HbA1c level (t=10.764), the differences were statistically significant (P＜0.05). Logistic regression analysis showed that longer AL [odds ratio (OR)=1.428, 95% confidence interval (CI) 1.054-1.934], DEX implantation in pars plana (OR=1.358, 95%CI 1.063-1.735), and higher HbA1c (OR=1.702, 95%CI 1.225-2.366) were the risk factors for secondary intraocular hypertension in DME patients after DEX treatment (P＜0.05), older age was a protective factor (OR=0.548, 95%CI 0.380-0.789, P＜0.05). ConclusionsLong AL, DEX implantation in pars plana and high HbA1c are the risk factors for secondary intraocular hypertension after DEX treatment in DME patients, older age is a protective factor.
Objective To analyze the protective effects of heat-shock response on the retinae of the rats after retinal ischemic reperfusion injury.Method Twenty Wistar rats (20 eyes) were divided into 4 groups: intracameral perfusion group (group P), intracameral perfusion after quercetin injection group (group P+Q), intracameral perfusion after heat shock group (group P+H), and in tracameral perfusion after quercetin injection and heat shock group (group P+Q+H ). According to the standard program established by International Society for Clinical Visual Electrophysiology, we recorded the results of the dark-adapted electroretinogram (D-ERG ),oscillatory potentials (OPs),and light-adapted ERG (L-ERG) of the rats with intraocular hypertension after induced by heat shock response. The expressions of HSP 70 of the rats in all groups were observed by Western blotting.Results The expression of HSP 70 of the rats in group P+H was the highest in all groups, but the expressions of HSP70 in group P+Q and P+Q+H were inhibited significantly. The amplitudes of a and b wave of ERG and O2 wave of OPs decreased, and the delitescence of them were delayed significantly in rats after intracameral perfusion. The amplitude of b wave of D-ERG and O2 wave of OPs in group P+H were higher than which in group P. Zero hour after perfusion, the amplitudes of all waves in group P+H increased significantly (Plt;0.05). Twenty-four hours after perfusion, the retinal functional resumption of the rats in group P+H was better than which in group P. In group P+Q and P+Q+H, the delitescences of all waves of ERG and O2 wave of OPs were the longest and the amplitudes were the lowest, and some waves even disappeared.Conclusions The heat-shock response may improve the recovery ability of the retinal cells after injury of ischemic reperfusion.(Chin J Ocul Fundus Dis，2003，19：117-120)
Objective To investigate the factors associated with short-term elevation of intraocular pressure after ranibizumab intravitreal injection. Methods 292 eyes of 292 patients who were diagnosed retinopathy and suitable to receive ranibizumab intravitreal injection were enrolled in this prospective clinical study. There were 157 males and 135 females. 193 patients diagnosed with age-related macular degeneration and 99 other retinopathy patients. Mean age of patients was 62.75±13.74 years. All subjects underwent systemic and comprehensive ophthalmology examinations. The mean BCVA was 0.68±0.47 logMAR. Mean basal intraocular pressure was 18.1 mmHg (1 mmHg=0.133 kPa). All patients received intravitreal injection with 0.05 ml of ranibizumab (0.5 mg). The intraocular pressure were measured by non-contact tonometer at 10, 30, 120 minutes and 1 day after injection in a sitting position. The patients were grouped by the changes of intraocular pressure 10 minutes after injection. The elevation was more than 10 mmHg as elevation group and less than 10 mmHg as stable group. Analyze the possible related factors with elevation of intraocular pressure after ranibizumab intravitreal injection by comparing the different datum of two groups. Results The mean intraocular pressure were 23.8, 20.5, 19.9 and 17.4 mmHg at 10, 30, 120 minutes and 1 day after injection. The significant elevation level were 5.8, 2.4, 1.8, −0.7 mmHg compared with basal intraocular pressure. Among 292 eyes, intraocular pressure elevation in 68 eyes and stabled in 224 eyes. The age (Z=−0.732), gender (χ2=1.929), right or left eye (χ2=2.910), BCVA (Z=−0.039), diseases (χ2=2.088) were no significant difference between two groups (P＞0.05). The injection number (Z=−2.413, P=0.001), basal intraocular pressure (Z=−3.405, P=0.016) and elevations after injection (Z=−11.501, −8.366, −5.135, −3.568; P＜0.01) were significantly different comparing two groups (P＜0.05). By logistic regression analysis, basal intraocular pressure was positively correlated with the elevation of intraocular pressure 10 minutes after injection (B=−0.844, OR=0.43, 95%CI 0.24−0.76, P=0.004). Patients with higher basal intraocular pressure may occur intraocular pressure elevation after ranibizumab intravitreal injection much probably. Conclusions The factors associated with short-term elevation of intraocular pressure after ranibizumab intravitreal injection were basal intraocular pressure. The higher basal intraocular pressure, the higher risk to gain elevation of intraocular pressure after injection.
In this paper,the changes of activities of enzymes relating toenergy metabolism in rabbit's retina during acute ocular hypertension were observed.The activities of succinate dehydrogenase and adenosine triphosphatase were foud to be reduced,while the activities of the lactatic dehydrognease and glucose-6-phosphatase increased.The results reveal the disturbance of metabolism of energy in retina undergone acute ocular hypertension,and suggest that this might be the underlying factors relating to the defects of the functions and structures of the retina. （Chin J Ocul Fundus Dis,1993,9:141-144）
Objective To observe the effects of minocycline to the viability and apoptosis of ratprime;s retinal neuron cells (RNC) under pressure, and to investigate the neuroprotective mechanisms of minocycline against the RNC damage. Methods Establish a model of ratprime;s RNs under pressure cultured in vitro, the protective effect of minocycline is observed by different methods, including observing the morphology of the cells, evaluating the cellsprime; viability by methyl thiazolyl tetrazolium (MTT) colorimetry assay, and detecting the cellular apoptosis with acridine orange/ethidium bromide (AO/EB) double staining by fluorescence microscopy. Immunocytochemistry was used to detect the expression of iNOS and caspase-3 in the cells. Results Obvious morphology changes of RNC were found in cells under pressure compared with the control; the viability of RNC decreased and cellular apoptosis was found in 53.93% cells. The cellular morphology improved in the cells treated by 20 mu;mol/L minocycline, the cellular viability significantly increased, and the cellular apoptosis was found in 17.29% cells. In addition, the expression of iNOS and caspase3 in the treated cells decreased compared with which in the pressured group. Conclusion Minocycline with a certain concentration can effectively inhibit pressureinduced damage and apoptosis of RNC of rats, and the inhibitory effect on expression of iNOS and capases-3 may be the underlying mechanism.
Objective To investigate the occurrence, progress and conversion of hypotony in anterior proliferative vitreoretinopathy (aPVR), and to provide knowledge about how to prevent and treat it． Methods Animal models of chronic hypotony by aPVR were made with cultured ho mologous dermal fibroblasts on pigmented rabbits．The intraocular pressure (IOP) and ultrasound biomicroscopy(UBM) examination were taken preoperatively and on days 7,14, 28 and 56 postoperatively．Rabbits were killed on days 14, 28 or 56 postoperatively, prepared for histology and ultrastructure examination． Results The average IOP of experimental group was lower than that of control group on days 7,14,28 and 56 significantly (Plt;0．01)．UBM demonstrated that trip like echo emerged in front of ciliary body four weeks postoperatively, and tractional retinal detachment was found four weeks and eight weeks postoperatively in experimental group． Microscopic examination showed atrophy orabsence of the non-pigmented ciliary epithelium on days 28 and 56 postoperatively in experimental group．Electronic microscopy showed that the amount of mitochondrions decreased and there were many vacuoles in the non-pigmented ciliary epithelium in experimental group four and eight weeks postoperatively． Conclusions Atrophic change of the non-pigmented epithelium due to dragging effect of the ciliary body from the epiciliary membrane in aPVR might be the main cause of hypotony． (Chin J Ocul Fundus Dis, 2001,17:216-220)