Objective To investigate the mRNA expression of ciliary neurotrophic factor on the retina during injury and repair of optic nerves in rats. Methods Thirty-five healthy SD rats were randomly divided into 3 groups: 5 in the control group, 15 in the simply transected optic nerve group and 15 in the optic nerve-sciatic nerve anastomosis group. The simply transected and optic nerve-sciatic nerve anastomosed models were set up, and the retinal tissues of all of the rats were taken out after 3, 7 and 14 days, respectively; and the mRNA expression of CNTF in the 3 groups were observed by semiquantitative reversal transcription-polymerase chain reaction method. Results A minimum expression of CNTF mRNA was found in the retinae of the control group, and the increased rates of expression were found in the retinae of the simple transection of optic nerve group with the increase rate of 100%, 594%, and 485% on the 3rd, 7th, and 14th day respectively after the operation, while in optic nerve-sciatic nerve anastomosis group, the increase rates were found to be 258%, 752% and 515% on the 3rd, 7th, and 14th day respectively after the operation. Conclusion Retinal neurons can respond to axonal reaction of retinal ganglion cells by up-regulate endogenous CNTF after the injury of the optic nerves, which may provide a theoretic base for the application of the exogenous CNTF. (Chin J Ocul Fundus Dis，2004，20：355-357)
Objective To explore the role of activated macrophage in the repair of traumatic optic nerve injury in an animal model of incomplete traumatic optic nerve injury with lens damage.Methods One hundred and twelve healthy New Zealand big ear white rabbits were divided into two groups (experimental and control groups) randomly. According to the different time points (one, four, seven, ten, 14, 21 and 28 days), each group was further divided into seven subgroups, each subgroup had eight rabbits. Traumatic optic neuropathy and lens damage were induced in one eye of each rabbit by fluid percussion brain injury device (FPI); those eyes were the experimental group. The eyes of control group only had traumatic optic neuropathy. The functional and morphological changes of retina and optic nerve were evaluated by histopathology and flashvisual evoked potential (FVEP).Results FVEP P100 latency was (42.74plusmn; 5.83) ms, P100 amplitude was (7.98 plusmn; 2.15) mu;V before optic nerve injury was induced. One day after the injury, the P100latency increased and the P100amplitude reduced significantly. The P100 latency reached the longest at ten days after injury, and then recovered gradually. The P100 amplitude reached the lowest at seven days after injury, and then recovered gradually. The histopathological examination showed activated macrophages were not detected in the retina and optic nerve at day one after the injury, then they increased gradually and reached their peak (91.25plusmn;6.91) at day ten, and decreased after that, the difference was statistically significant (F=21.277, P=0.000); retinal ganglion cell axon regeneration began at day seven after the injury with an average of (6.38plusmn;1.85). The axons increased gradually and reached their peak (49.63plusmn;2.50) at day 28, and the changes were significant (F=7.711, P=0.000). Conclusions Incomplete optic nerve injury can recover gradually if there is lens damage at the same time. Activated macrophage may play an important role in this recovery process.
ObjectiveTo observe the early ultrastructural changes of the optic nerves after the brain impact injury.MethodsEighteen 15-week-old Wistar rats were used in the air-pressure brain impact injury examination. All of the rats underwent the procedures of right-parietal-bone fenestration after abdominal cavity anesthesia with 1% sodium pentolbarbital (45 mg/kg), and then they were divided randomly into 3 groups, i.e., mild injury group (8 rats) underwent with 7 kg of air pressure in distance of 11 cm; severe injury group (8 rats) with 7 kg of airpressure in distance of 8 cm; and control group (2 rats) underwent with the parietalbone fenestration but without impact injury.The ultrastructural changes of the optic nerves were observed 1, 6, 24, and 72 hours after the injury by electron microscopy.ResultsThe difference of ultrastructural changes of optic nerve was not obvious in wild injury group and the control group, and the lanthanum nitrate was only found in the blood vessels in optic nerve. The lanthanum nitrate entered the nerve stroma 1 hour after severe and increased as time goes on. Simultaneously, displayed dilatation of endoplasmic reticulum, cavitation and tumefaction of mitochondrion, vacuolation of nerve stroma, and vacuolation of some axis-cylinder were seen in the glial cells.ConclusionThe brain impact injury may cause ultrastructural changes of the optic nerve and increase of permeability of blood vessels. (Chin J Ocul Fundus Dis, 2005,21:41-43)
The neuroretinal injuries of diabetic retinopathy (DR) include retinal neuronal damage and reactive gliosis, both of which are induced by hyperglycemia and presented as early features of DR. They promote to develop mutually and accelerate the progression of DR. The molecular mechanisms study of neuronal damage mainly focuses on the alterations of extracellular environment and related signaling pathways, include inflammation, oxidative stress, endoplasmic reticulum stress, the formation of advanced glycation end products, glutamate toxicity and so on. These alterations mainly result in neuronal apoptosis and autophagy. The damaged neurons activate the glial cells with apparent changes in morphology, cell counts and the level of intracellular protein expression. In non-proliferative DR, glial cells are moderately hypertrophic and slightly increased in numbers. In proliferative DR, there is a significant rise in glial cell number with enhanced level of inflammatory factors and vascular active substances which lead a further neuronal damage. Signaling pathways of extracellular signal-regulated kinase 1/2, c-Fos and p38 mitogen-activated protein kinase are associated with their activation. Researches on the molecular mechanisms and signaling pathways of the DR will promote controlling the DR progression at the cellular level.
Objective To evaluate the influence of the location of retinal vessel trunk on neuroretinal rim width of inferior and superior sectors of optic disc, and explore its role in the diagnosis of glaucomatous optic nerve lesion. Methods The photographs of ocular fundus from 459 patients with clear location of retinal vessel trunk, including large disc in 131, medium disc in 145, horizontally oval disc in 75, and small disc in 108 were evaluated. Independent-sample t test was used to compare the difference of the superior and inferior rim widths between the higher-vessel group and the lower-vessel group, and to compare the difference of superior and inferior vessel distances between the narrow-superior-rim-width group and the narrow inferior-rim-width group. Results In most of the patients, or the ones with large and small disc, the ratio of superior rim width to summation of superior and inferior rim widths in the higher-vessel group（0.467plusmn;0.051，0.445plusmn;0.040，0.508plusmn;0.056）were less than which in the lowervessel group（0.500plusmn;0.066，0.474plusmn;0.062，0.546plusmn;0.048）, and the differences were significant（P=0.000, 0.045, 0.018）; the ratio of superior vessel distance to summation of superior and inferior vessel distance in the narrow-superior-rim-width group（0.510plusmn;0.051，0.508plusmn;0.055，0.512plusmn;0.036）were less than which in the narrow-inferior-rim-width group（0.528plusmn;0.045，0.533plusmn;0.048，0.534plusmn;0.045）, and the differences were significant（P=0.000, 0.046, 0.022）. Conclusions The position of optic disc vessel trunk influences its superior and inferior rim width. The rim closer to vessel trunk position has narrower width than which comparatively far away from the position. In patients with large, medium, horizontally oval optic disc, glaucoma optic nerve lesion would be considered if the optic disc has the shape of narrower inferior rim, broader superior rim, and vessel location in the superior half of the disc. In the ones with small disc, the optic disc with the shape of narrower superior rim, broader inferior rim, and vessel location in the inferior half of the disc may suggest glaucoma optic nerve lesion. (Chin J Ocul Fundus Dis, 2007, 23: 118-121)
ObjectiveTo investigate the effect of nerve growth factor (NGF) on recuperate of optic nerve after contusion by clamping in adult rabbits. MethodsSixteen adult rabbits were randomly divided into NGF and the control group with 8 rabbits in each group. After the optic nerve of the right eyes was clamped，tissue engineering nerve containing 0.06 ml NGF（concentration: 5×10-4 g/L, NGF group） and 0.06 ml of PBS (control group) was immediately transplanted into the injured eyes respectively, and 0.02 ml NGF（concentration: 5×10-4 g/L, NGF group）and 0.02 ml of PBS (control group) were injected into the vitreous of right eyes respectively. Flash visual evoked potential (FVEP) test was performed on the eyes 1 day, 2 weeks and 8 weeks after the injury. The number of retinal ganglion cells (RGCs) and changes of optic nerves were observed by light microscopy and electron microscopy at the 8th week after contusion,and a computer-image-analysis system was used to count the optic nerve axons.ResultsThe ratio of amplitude of FVEP of the injured and healthy eyes was 0.765±0.150 in NGF group and 0.494±0.108 in the control at the 2th week after injury with a significant difference between the two groups (Plt;0.05); and was 0.581±0.138 and 0.409±0.119 respectively at the 8th week after contusion with statistical difference between the two groups (Plt;0.05). The results of light microscopy and electron microscopy showed that degeneration of RGCs and optic nerves in the NGF group was lighter than that in the control group 8 weeks after injury, while the amount of optic nerve axons was (10 955±608.7) axons/ mm2 in the NGF group and (7 898±608.8) axons/mm2 in the control with statistical difference between the two groups (Plt;0.05). ConclusionNGF may redound to the survival of RGCs and regeneration of the axons in some degree, which can promote the recuperation of optic nerve and visual function. (Chin J Ocul Fundus Dis, 2005,21:253-257)
Objective To observe the content of thromboxane (TXA2 ) and prostacyclin (PGI2) in optic nerves after forehead impact injury.Methods The right forehead zones of 32 rabbits were struck by biology impact machine. Tweenty-four rabbits that had afferent papillary defect after injury were chosen, and randomly divided into four groups: 1 day, 2, 4, and 7 days group. Right eyes were in the experimental group and left eyes were in the control group. Flash visual evoked potentials were examined before and after the traumatic injury. The rabbits ′eyes were removed, the optic nerves were pathologically examined, and the content of TXB2 and 6-Keto-PGF1αwhich were the products of TXA2 and PGI2 were assayed 1, 2, 4, and 7 days after traumatic injury respectively.Results Histopath ological examination revealed the findings of injuries of optic nerves of all the 24 rabbits. The latency of wave P1 was significantly delayed after traum atic injury (Plt;0.01), and amplitude of wave P1 was significantly decreased after traumatic injury (Plt;0.01). The content of TXB2 ［(172.35±26.52) pg/mg ］and 6-Keto-PGF1α［(161.78±24.83) pg/mg］were significantly higher in the injured optic nerves than in the uninjured ones 1 day after the traumatic injury (Plt;0.01). The rate of TXB2 /6-Keto-PGF1α (1.077±0.18) was significantly increased compared to the control group (Plt;0.05), and lasted to the 7th day.Conclusions The content of TXA2 and PGI2 significantly increases and the ratio of them is lopsided after forehead impact injury in rabbits. (Chin J Ocul Fundus Dis，2003，19：49-51)
Purpose To evaluate differences in the pattern of optic disc and retinal nerve fiber layer (RNFL) damage in normal-tension glaucoma (NTG) and high-tension glaucoma (HTG) patients. Methods We enrolled 49 eyes of 49 patients:30 NTG (IOP≤21 mm Hg,1 mm Hg=0.133 kPa), 19 HTG(IOP≥25 mm Hg). Mean age was 59.2±12.3 (range, 36-75) for HTG patients, and 59.6±8.6(range, 39-71) for NTG patients. All patients underwent complete ophthalmic examination, achromatic automated perimetry (AAP), scanning laser ophthalmoscopy (SLO), scanning laser polarimetry (SLP), optical coherence tomography (OCT) and Heidelberg retinal tomography (HRT). All patients had glaucomatous optic nerve damage and abnormal AAP. Results There were no differences in mean deviation on AAP between NTG and HTG eyes (P=0.37), while the corrected pattern standard deviation was larger in NTG than in HTG eyes (P=0.014). Cup∶disc area ratios in global (P=0.03) and three sectors (Plt;0.05) except nasal sector were significantly larger in the NTG group, whereas rim area in global (P=0.03) and three sectors (Plt;0.05) except nasal quadrant obtained by SLO were smaller in NTG than in HTG eyes. The other numerical parameters obtained by three imaging technologies could not detect differences in the optic disc or RNFL anatomy between the two groups. Conclusions Cup∶disc area ratio was larger in patients with NTG than in those with HTG, whereas significant thinning of rim was associated with NTG eyes. The measurement of retinal nerve layer thickness in global and each quadrant was similar between two groups. More focal or segmental analysis of the data contained within SLO, SLP and OCT images are needed to detect localized differences in eyes with varying levels of IOP. (Chin J Ocul Fundus Dis, 2002, 18: 109-112)
ObjectiveTo investigate the effect of DJ-1 encoded by Park7 gene on retinal ganglion cells (RGC) and visual function after optic nerve crush injury (ONC) in mice.MethodsThirty-seven and 116 healthy male C57BL/6J mice were randomly divided into group normal, group ONC 2d, group ONC 5d, group ONC 7d and group control, group Park7, group Park7-ONC, group ONC and group green fluorescent protein (GFP)-ONC. Group ONC 2d, group ONC 5d and group ONC 7d were sacrificed on the 2nd, 5th and 7th day after the establishment of ONC model, and the follow-up experiments were carried out. The mice in group Park7 and group Park7-ONC were injected 1 μ recombinant adeno-associated virus (rAAV) with knocking down Park7 gene into vitreous cavity, and 1 μ l rAAV with only GFP was injected into vitreous cavity of mice in group GFP- ONC, and virus transfection was observed 4 weeks after injection. The injury of ONC was perfomed at 23 days after vitreous injection in group ONC, group Park7-ONC and group GFP-ONC, and the samples were taken for follow-up experiment 5 days after modeling. The average density of RGC was observed by immunofluorescence staining, the latencies and amplitudes of a-wave, b-wave and photopic negative response (phNR) and the amplitude of oscillatory potential (OPs)were detected by full-field flash electroretinogram,and the visual acuity of mice was measured by optomotor response (OMR). The relative expression levels of DJ-1, Bax and B lymphoblastoma / leukemia-2 (Bcl-2) protein in the retina of mice in each group were detected by Western blot. One-way ANOVA was used to compare the data between groups, and t-test was used for pairwise comparison between groups.ResultsCompared with the normal group, the relative expression of DJ-1 protein in the retina of the ONC 2 d group and ONC 5 d group increased significantly, and the difference was statistically significant (t=16.610, 5.628, P＜0.01,＜0.05). Four weeks after virus transfection, strong GFP expression was seen in the RGC layer and inner plexiform layer of the retina of mice in the Park7 group. Compared with the control group, the RGC density of the retina in the ONC group decreased significantly, and the difference was statistically significant (t=16.520, P＜0.000); compared with the ONC group, the RGC density of the retina in the Park7-ONC group decreased significantly, and the difference was statistically significant (t=6.074, P＜0.01). With the increase of stimulus light intensity, the dark adaptation a wave and b wave latency of the mice in the control group gradually shortened, and the amplitude gradually increased. The stimulus light intensity was 3 cd·s/m2. There was no statistically significant difference in the dark adaptation a wave and b wave latency and amplitude of the control group, Park7 group, Park7-ONC group, ONC group, and GFP-ONC group (Incubation period: F=0.503, 2.592; P=0.734, 0.068. Amplitude: F=0.439, 1.451; P=0.779, 0.247). Compared with the control group, the Ops and PhNR amplitudes of the ONC group mice were significantly decreased (t=15.07, 12.80; P＜0.000,＜0.001). Compared with the ONC group, the Ops and PhNR amplitudes of the mice in the Park7-ONC group were significantly decreased (t=4.042, 5.062; P＜0.05,＜0.01); there was no statistically significant difference in the PhNR latency of the mice in each group (F=1.327, P=0.287). Compared with the control group, the visual acuity of the mice in the ONC group was significantly decreased, and the difference was statistically significant (t=23.020, P＜0.000); compared with the ONC group, the visual acuity of the mice in the Park7-ONC group was significantly decreased, and the difference was statistically significant (t=3.669, P＜0.05). Compared with the control group, Park7-ONC group and ONC group, the relative expression of DJ-1 protein in the mouse retina was significantly down-regulated, and the difference was statistically significant (t=47.140, 26.920; P＜0.000,＜0.000). There was no significant difference between ONC group and GFP-ONC group (t=0.739, P=0.983). Compared with the ONC group, the relative expression of Bax protein in the mouse retina of the Park7-ONC group was significantly increased, and the relative expression of Bcl-2 protein was significantly reduced. The differences were statistically significant (t=5.960, 9.710; P＜0.05,＜0.05); the relative expression ratio of Bcl-2/Bax in the Park7-ONC group was significantly lower than that in the ONC group, and the difference was statistically significant (t=13.620, P＜0.01).ConclusionThe expression of DJ-1 encoded by Park7 gene is down-regulated after Park7 gene was knocked down, which aggravates the RGC damage and the decrease of retinal electrophysiological response and visual function in ONC injury mice.