ABSTRACT
AIM: To evaluate the changes of retinal microvascular density in patients with sellar region tumor, and its correlation with the damage to visual field, and to explore its application value in evaluating optic nerve injury of those patients.METHODS: Cross-sectional study. A total of 157 patients(292 eyes)with sellar region tumor, including 82 cases(152 eyes)of pituitary adenoma and 75 cases(140 eyes)of craniopharyngioma, were selected from neurosurgery department and ophthalmology department of Beijing Tiantan Hospital, Capital Medical University between October 2018 and May 2022. A total of 90 people(180 eyes)during the same period, including the family members of patients, students and staff in Beijing Tiantan Hospital, Capital Medical University were collected as control group. All participants underwent optical coherence tomography angiography(OCTA)examination. The changes of retinal microvascular density and its correlation with visual field parameters were compared between the two groups.RESULTS: In patients with sellar region tumor, the radial peripapillary capillary(RPC)and superficial retinal capillary plexus(SRCP)density were significantly lower than that in the control group [50.81%(46.49%, 53.49%)vs. 52.78%(50.73%, 54.51%)and 50.57%(48.13%, 52.73%)vs. 51.63%(49.78%, 53.02%), all P<0.05]. The RPC density in the craniopharyngioma group was lower than that in the pituitary adenoma group [49.71%(44.33%, 53.14%)vs. 51.37%(47.42%, 53.95%), P<0.05]. The MD, PSD and VFI of the sellar region tumor group were -4.33(-12.22, -1.85)dB, 3.37(1.91, 8.82)dB and 92%(65%, 97%)respectively. RPC density of patients with sellar region tumor was positively correlated with MD and VFI, and was negatively correlated with PSD. The SRCP density of each quadrant was positively correlated with MD, and was positively correlated with VFI except Para-T and it was negatively correlated with PSD(all P<0.05).CONCLUSION: Retinal microvascular changes were present in patients with sellar region tumor. Lower vessel density indicates more severe damage to visual field. In the clinic, visual field examinations combined with OCTA were helpful to find the optic nerve injury of patients.
ABSTRACT
Glaucomatous optic neuropathy(GON)is the difficulty of glaucoma treatment. In recent years, a variety of theories have been put forward about the pathogenesis of GON, but none of them can explain the principle of optic neuropathy caused by all types of glaucoma, which makes the disease difficult to treat in clinical treatment and is not conducive to early intervention. The latest research found that the transient receptor potential channel vanillic acid subfamily 4(TRPV4)in the retina plays an important role in various pathogenesis of GON. This article will review TRPV4 and its role in the occurrence and development of GON in order to find a common “connection point” for the multiple mechanism theories of GON, which will contribute to further understanding and clinical treatment of the disease.
ABSTRACT
ABSTRACT Purpose: To examine changes in the eyes after cold compress application at the early stage. Method: A total of 62 eyes from 62 healthy adult participants were included in this cross-sectional and comparative study. The subfoveal choroidal thickness and retinal nerve fiber thickness were measured by spectral-domain ocular coherence tomography. The central corneal thickness, anterior segment volume and depth, iridocorneal angle, and pupil diameter were measured by means of the Scheimpflug anterior segment imaging method. The measurements were repeated after 10 min of cold compress application, which was applied using special packs. The procedures were then repeated with non-cold packages to exclude the effect of pressure. Results: The average age of the participants was 30.74 ± 5.82 years. There was no significant change in the central corneal thickness after cold compress application, and there was a significant decrease in the anterior segment volume (p<0.001), anterior segment depth (p<0.001), and pupil diameter. Moreover, the iridocorneal angle increased (p=0.002). The subfoveal choroidal thickness decreased after the application of cold compress (p<0.001). The overall disk thickness (p=0.034) and superior nasal scale (p=0.007) significantly decreased after the cold compress was administered during the evaluation of optic nerve fiber thickness. In contrast to that with the cold application, the subfoveal choroidal thickness and optic nerve fiber thickness did not change after the non-cold compress application (p>0.05). Conclusion: Cold compress application may thus cause some physiological changes in the eyes, which necessitates the examination of its usage and effects.
RESUMO Objetivos: Examinar as mudanças nos olhos após a aplicação com compressa fria. Método: Sessenta e dois olhos de 62 adultos saudáveis foram incluídos neste estudo transversal e comparativo. A espessura da coróide subfoveal e a espessura da fibra nervosa retiniana foram mensuradas por tomografia de coerência óptica de domínio espectral (OCT). A espessura central da córnea, o volume e a profundidade do segmento anterior, o ângulo iridocorneano e o diâmetro da pupila foram mensurados por meio do método de imagem do segmento anterior de Scheimpflug. As medições foram repetidas após 10 minutos de aplicação de compressas frias, aplicadas com embalagens especiais. Os procedimentos foram repetidos com embalagens não frias para excluir o efeito da pressão. Resultados: A média de idade dos participantes foi de 30,74 ± 5,82 anos. Embora não tenha havido alteração significativa na espessura central da córnea após a aplicação da compressa fria, houve diminuição significativa no volume do segmento anterior (p<0,001), na profundidade do segmento anterior (p<0,001) e no diâmetro da pupila. Além disso, o ângulo iridocorneano aumentou (p=0,002). A espessura da coróide subfoveal diminuiu após a aplicação da compressa fria (p<0,001). A espessura total do disco (p=0,034) e a escala nasal superior (p=0,007) diminuíram significativamente após a administração da compressa fria durante a avaliação da espessura da fibra do nervo óptico. Ao contrário da aplicação com compressa fria, a espessura da coróide subfoveal e a espessura da fibra do nervo óptico não mudaram após a aplicação da compressa não fria (p>0,05). Conclusão: A aplicação de compressa fria pode causar algumas alterações fisiológicas nos olhos e o seu uso e efeitos devem ser observados.
ABSTRACT
Purpose: There are no effective treatments currently available for optic nerve transection injuries. Stem cell therapy represents a feasible future treatment option. This study investigated the therapeutic potential of human umbilical cord–derived mesenchymal stem cell (hUC?MSC) transplantation in rats with optic nerve injury. Methods: Sprague–Dawley (SD) rats were divided into three groups: a no?treatment control group (n = 6), balanced salt solution (BSS) treatment group (n = 6), and hUC?MSCs treatment group (n = 6). Visual functions were assessed by flash visual evoked potential (fVEP) at baseline, Week 3, and Week 6 after optic nerve crush injury. Right eyes were enucleated after 6 weeks for histology. Results: The fVEP showed shortened latency delay and increased amplitude in the hUC?MSCs treated group compared with control and BSS groups. Higher cellular density was detected in the hUC?MSC treated group compared with the BSS and control groups. Co?localized expression of STEM 121 and anti?S100B antibody was observed in areas of higher nuclear density, both in the central and peripheral regions. Conclusion: Peribulbar transplantation of hUC?MSCs demonstrated cellular integration that can potentially preserve the optic nerve function with a significant shorter latency delay in fVEP and higher nuclear density on histology, and immunohistochemical studies observed cell migration particularly to the peripheral regions of the optic nerve.
ABSTRACT
Traumatic optic neuropathy and glaucoma can cause optic nerve degenerative changes leading to a significant decline in vision, which seriously affects the quality of life of patients.In recent years, research on mammalian optic nerve injury models has found that optic nerve injury involves pathophysiological processes such as apoptosis, inflammatory response, and oxidative stress.Researchers have explored the relevant mechanisms and regulatory signaling pathways of optic nerve injury, and have conducted research on the protection of optic nerve injury in the fight against retinal ganglion cell (RGC) apoptosis, new drug therapy, gene therapy, stem cell transplantation and natural extracts.Studies have shown that glucose regulatory protein 75, a member of the heat shock protein 70 family, and melatonin naturally secreted in the human retina may play an important role in the regulation of RGC apoptosis.Human granulocyte colony-stimulating factor (G-CSF) may play a protective role in RGC by directly activating the intrinsic G-CSF receptor and downstream signaling pathway.Targeting gene therapy is expected to become a powerful therapy for repair and regeneration of injured optic nerve.Adipose stem cell transplantation can resist the apoptosis of retinal cells in rat model.In addition, lycium barbarum polysaccharide can delay the secondary degeneration of axons, which may be a promising natural extract to delay the secondary degeneration of optic nerve injury.This article summarized the mechanism, regulation and protection of optic nerve injury.
ABSTRACT
@#AIM: To investigate the expression changes of Toll like recepter 9(TLR-9)and myeloid differentiation factor 88(MyD88)in retina of mice following optic nerve injury(ONI).<p>METHODS: There were 36 male 8-week-old C57BL/6J mice randomly divided into 6 groups: blank control(no treatment), ONI 1d group(materials were taken at 1d after optic nerve injury), ONI 3d group(materials were taken at 3d after optic nerve injury), ONI 5d group(materials were taken at 5d after optic nerve injury), ONI 7d group(materials were taken at 7d after optic nerve injury), ONI 14d group(materials were taken at 14d after optic nerve injury). The mice optic nerve model was made by optic nerve gripping, and the mRNA and protein levels of Toll like recepter 9 and myeloid differentiation factor 88 in each retinal were measured by RT-qPCR and Western-blot.<p>RESULTS: The mRNA and protein levels of Toll like recepter 9 and myeloid differentiation factor 88 in the retina of ONI 1d group were not significantly different from those of the blank control group(<i>P</i>>0.05), the mRNA and protein levels of TLR-9 and MyD88 in the retina of ONI 3d group, ONI 5d group, ONI 7d group and ONI 14d group were significantly increased compared with the blank control group, and the differences were statistically significant(<i>P</i><0.01). Compared with the blank control group, the mRNA and protein levels of TLR-9 and MyD88 in the retina of mice began to increase at ONI 3d(<i>P</i><0.01), peaked at ONI 5d(<i>P</i><0.001), and gradually decreased at ONI 7d(<i>P</i><0.01).<p>CONCLUSION: Optic nerve injury can activate the expression of TLR-9 and MyD88 in mice retina. TLR-9 and MyD88 may play an essential role in the process of optic nerve injury.
ABSTRACT
OBJECTIVES@#To study the quantitative and qualitative differences of visual evoked potential (VEP) in monocular visual impairment after different parts of visual pathway injury.@*METHODS@#A total of 91 subjects with monocular visual impairment caused by trauma were selected and divided into intraocular refractive media-injury group (eyeball injury group for short), optic nerve injury group, central nervous system injury and intracranial combined injury group according to the injury cause and anatomical segment. Pattern Reversal visual evoked potential (PR-VEP) P100 peak time and amplitude, Flash visual evoked potential (F-VEP) P2 peak time and amplitude were recorded respectively. SPSS 26.0 software was used to analyze the differences of quantitative (peak time and amplitude) and qualitative indexes (spatial frequency sweep-VEP acuity threshold, and abnormal waveform category and frequency) of the four groups.@*RESULTS@#Compared with healthy eyes, the PR-VEP P100 waveforms of the intraocular eyeball injury group and the F-VEP P2 waveforms of the optic nerve group showed significant differences in prolonged peak time and decreased amplitude in injured eyes (P<0.05). The PR-VEP amplitudes of healthy eyes were lower than those of injured eyes at multiple spatial frequencies in central nervous system injury group and intracranial combined injury group (P<0.05).The amplitude of PR-VEP in patients with visual impairment involving central injury was lower than that in patients with eye injury at multiple spatial frequencies. The frequency of VEP P waveforms reaching the threshold of the intraocular injury group and the optic nerve injury group were siginificantly different from the intracranial combined injury group, respectively(P<0.008 3), and the frequency of abnormal reduction of VEP amplitude of threshold were significantly different from the central nervous system injury group, respectively(P<0.008 3).@*CONCLUSIONS@#VEP can distinguish central injury from peripheral injury, eyeball injury from nerve injury in peripheral injury, but cannot distinguish simple intracranial injury from complex injury, which provides basic data and basis for further research on the location of visual impairment injury.
Subject(s)
Humans , Evoked Potentials, Visual , Eye , Optic Nerve , Optic Nerve Injuries , Vision Disorders/etiologyABSTRACT
@#AIM: To analyze the protective effect of resveratrol on the optic nerve of glaucoma rats and its effect on the phosphatidylinositol 3 kinase(PI3K)/protein kinase B(Akt)signal pathway and its related factors.<p>METHODS: SPF grade SD rats were used to cauterize the scleral surface veins to make a right eye glaucoma model. After successful modeling, different doses(10, 20, 40 mg/kg intraperitoneal injection)of resveratrol were used to intervene. Intraocular pressure was measured 2h after the last administration, and retinal slices were made to observe the survival of retinal ganglion cells(RGC). Retinal plaque to observe the survival of retinal ganglion cells(RGC). Real-time fluorescence quantitative PCR and Western blot were used to detect the mRNA and protein expression of retinal PI3K, Akt, basic fibroblast growth factor(bFGF), and brain-derived neurotrophic factor(BDNF).<p>RESULTS: The intraocular pressure(30.25±4.25)mmHg in the model group was higher than that in the low-dose group(26.30±4.05)mmHg, the middle dose group(22.31±3.68)mmHg and the high dose group(18.32±3.21)mmHg, and the model group RGC labeling rate(48.25±4.50)% was lower than the low dose group(56.32±5.05)%, middle dose group(66.03±6.68)% and high dose group(78.56±7.82)%(<i>P</i><0.05). The intraocular pressure in the low, middle and high dose groups decreased in a dose-dependent manner, and the RGC labeling rate increased in a dose-dependent manner(<i>P</i><0.05). The p-PI3K/PI3K, p-Akt/Akt protein ratio, bFGF, BDNF mRNA and protein relative expression in the model group were lower than those in the low dose group, middle dose group, and high dose group(<i>P</i><0.05), and the low-dose group, middle dose group and high-dose group increased in a dose-dependent manner.<p>CONCLUSION: Resveratrol can inhibit the apoptosis of RGC in glaucoma rats and reduce optic nerve damage, which may be related to the up regulation expression of phosphorylated of related proteins in PI3K/Akt signal pathway and the expression of protective gene and protein of optic nerve.
ABSTRACT
Glaucoma is a common blinding eye disease characterized by progressive loss of retinal ganglion cells （RGCs） and their axons， gradual loss of visual field， and optic atrophy. The pathological changes of glaucoma are mainly the degeneration， atrophy， and loss of RGCs and their axons， which can eventually lead to the permanent impairment of visual function. The specific pathogenesis of glaucoma remains unclear. Autophagy is a process in which damaged， denatured， or senescent proteins and organelles are transported to lysosomes for digestion and degradation in order to continuously renew and rebuild cells for reuse. As revealed by clinical case analysis and animal experiments， Chinese patent medicine and some traditional Chinese medicine （TCM） therapies may be able to target the autophagy pathway. This paper expounded the role of autophagy in glaucoma-induced ocular hypertension and optic nerve injury from the aspects of stress response of ocular tissue to high intraocular pressure， trabecular meshwork dysfunction， immune regulation， and scar regulation as well as the regulatory effects of some Chinese medicinal ingredients on autophagy， aiming to explore the possibility of integrated TCM and western medicine in regulating autophagy and preventing glaucoma-induced optic nerve injury and early visual field loss. It was found that Chinese medicinal monomers or extracts function via multiple pathways and multiple targets， mainly involving two classical autophagy pathways， namely phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） and adenosine monophosphate-activated protein kinase （AMPK）. Moreover， the current studies on the neuroprotective effect of TCM mostly focus on the brain and spinal cord lesions of the central nervous system， and its protective mechanism against optic nerve injury in glaucoma still needs further investigation. In addition， autophagy was like a "double-edged sword" in different experimental animal models and methods. How to artificially intervene in autophagy to prevent the apoptosis of RGCs and protect the optic nerve injury is still an urgent problem to be solved in the future research.
ABSTRACT
@#AIM: To explore the value of frequency threshold optical coherence tomography(OCT)in the diagnosis of primary open angle glaucoma optic nerve injury. <p>METHODS: Eighty patients with early primary glaucoma who were admitted to the hospital between January 2018 and March 2020 and 100 healthy subjects were selected as the study subjects. Patients with primary open angle glaucoma were divided into early group, middle group and late group. OCT was used to measure the thicknesses of upper, lower, nasal, bitemporal peri-papillary retinal nerve fiber layer(pRNFL)and upper and lower macular ganglion cell complex(mGCC)in each group. The mean deviation(MD)of visual field was determined through perimetry. The OCT parameters and perimetry parameters were compared among groups. Spearman correlation analysis was performed to analyze the correlation between OCT parameters and visual field defects, and the receiver operating characteristic(ROC)curve was used to calculate the value of OCT parameters in diagnosing primary open angle glaucoma. <p>RESULTS: There were 24 cases, 39 cases and 17 cases in the early group, middle group and late group, respectively. There were statistically significant differences in pRNFL and mGCC among 3 groups(<i>P</i><0.05).The upper, lower, average pRNEL and the upper, lower, and average mGCC of patients in the early group of a third-class hospital were significantly lower than those of the control group, and the parameters of pRNFL and mGCC in each position of the mid-stage and late group were significantly lower than those of the control group. The upper, lower, nasal pRNFL, average pRNFL, upper, lower and average mGCC of the late group of glaucoma patients were significantly lower than those of the early group and the middle group. The indicators of the middle group were significantly lower than those of the early group(<i>P</i><0.05). Spearman correlation analysis showed that pRNFL and mGCC parameters were negatively correlated with glaucoma severity(<i>P</i><0.05)ROC curve analysis showed that the areas under the curves of the upper, lower, nasal, bitamporal and average pRNFL for diagnosis of primary open angle glaucoma optic nerve injury were 0.693, 0.846, 0.676, 0.579 and 0.844, respectively. The areas under the curves of upper, lower and average mGCC for diagnosis of primary open angle glaucoma optic nerve injury were 0.542, 0.677 and 0.676 respectively. The area under the curve of average pRNFL combined with average mGCC for the diagnosis of primary open angle glaucoma optic nerve injury was 0.883. <p>CONCLUSION:The pRNFL and mGCC measured by OCT are closely related to the degree of primary open angle glaucoma optic nerve injury. Both have high diagnostic value for glaucoma and can be used clinically for diagnosis and condition assessment.
ABSTRACT
Resumo As alterações congênitas do nervo óptico são raras. A hipoplasia é a forma mais comum de alteração congênita do nervo óptico. Acredita-se que seja correlacionada à interrupção do desenvolvimento fetal e ao baixo peso ao nascer. Apresenta-se como uma anomalia não progressiva com acuidade visual geralmente preservada. Relatamos um caso de uma paciente com hipoplasia segmentar superior com hipertensão ocular após uso de corticoide, cursando com diminuição da camada de fibras nervosas. Os pacientes portadores de hipoplasia devem ser acompanhados com mais rigor caso tenham fatores de risco para glaucoma e deve ser considerada como um diagnóstico diferencial para o glaucoma de pressão normal.
Abstract Introduction: Congenital changes of the optic nerve are rare. Hypoplasia is the most common form of congenital alteration of the optic nerve. It is believed to be correlated with interruption of fetal development and low birth weight. It presents as a non-progressive anomaly with generally preserved visual acuity. We related a case of a patient with superior segmental hypoplasia with ocular hypertension after corticosteroid use, with a decrease in the nerve fiber layer. Patients with hypoplasia should be followed more closely if they have risk factors for glaucoma and should be considered as a differential diagnosis for normal pressure glaucoma.
Subject(s)
Humans , Female , Adult , Glaucoma/diagnosis , Diagnosis, Differential , Optic Nerve Hypoplasia/diagnosisABSTRACT
@#Microglia are the resident macrophages of the central nervous system(CNS). Microglia constantly monitor the pathological changes of the surrounding microenvironment. Activated microglia play key roles in tissue protection and injury under the stimulation of various injury factors. Abnormal activation of microglia mediates retinal inflammation and aggravates the original ophthalmic diseases. Our growing understanding of the mechanisms of the interaction between microglia and retinal cells is identifying potential cellular and molecular targets for therapeutic interventions that may be apply to optic nerve injury, diabetic retinopathy, glaucoma and other diseases in the future. In this review, potential links between ophthalmic diseases and microglial activity will be explored.
ABSTRACT
@#Glaucoma is a kind of irreversible blind disease characterized by atrophyand depression of optic papilla, visual field defect and vision decline. The essence of optic nerve injury is the death of optic ganglion cells. Although controlling intraocular pressure through drugs and surgery can play a certain role in the treatment of glaucoma, how to fundamentally prevent the further development of glaucoma is still in the exploratory stage. Therefore, studying the mechanism of optic nerve injury in glaucoma is very important to treat glaucoma. In recent years, the immune mechanism on optic nerve injury in glaucoma has become a hot. In this paper, how TLR4 induces optic nerve injury in glaucoma patients was reviewed, with different immune pathways and interaction with the neuroglial.
ABSTRACT
@#Optic nerve injury is a common nervous system disease. Its basic pathological features are axonal degeneration and apoptosis of retinal ganglion cells(RGCs), which causes numbers of symptoms including visual dysfunction. Axonal degeneration, including axonal selective degradation, Wallerian degeneration induced by axonal transection, and apoptosis-induced axonal degeneration(axonal apoptosis), is an important part of neurodevelopment, axonal remodeling, and injury response process. Axonal degeneration is one of the initial steps in many traumatic neurological disorders, and damaged axons are generally unable to regenerate, which leads to neuronal cell apoptosis. Neuronal apoptosis causing the degeneration of both cell bodies and axons commonly occurs during the development of brain, as a result of various neuronal damages. Studies in recent years have confirmed that calcium is the main regulator of axonal degeneration. When an optic nerve crush(ONC)occurs, the degree of acute axonal degeneration(AAD)can be reduced by using calcium channel inhibitors to prevent the influx of calcium ions into axons, which will also improve the survival rate of RGCs and accelerate the regeneration of axons.
ABSTRACT
@#AIM: To investigate the correlation between NLRP3 inflammation and optic nerve injury in primary open-angle glaucoma(POAG). <p>METHODS: Totally 65 POAG patients(98 eyes)in our hospital from May 2016 to May 2017 were selected, meanwhile 30 cataract patients(49 eyes)were as control group. Visual impairment was judged according to the mean defect value(MD)and divided into mild(group A), moderate(group B)and severe(group C)groups. The quality of IL-1β and IL-18 in plasma was detected by ELISA, and proportion of NLRP3, ASC and Caspase-1 positive macrophages was measured by flow cytometry. <p>RESULTS: The levels of IL-1β and IL-18 and the proportion of NLRP3, ASC and Caspase-1 positive cells in POAG group were obviously higher than those in control group(<i>P</i><0.05). The levels of IL-1β and IL-18 and the proportion of NLRP3, ASC and Caspase-1 positive cells in group C were highest in subgroups(<i>P</i><0.05). The serum levels of IL-1β and IL-18 in POAG patients were positively correlated with visual field injury(<i>r</i>=0.432, 0.765), and the proportion of positive cells of NLRP3, ASC and Caspase-1 was positively correlated with visual field injury(<i>r</i>=0.517, 0.481, 0.340). <p>CONCLUSION: Serum levels of IL-1β, IL-18 and the proportion of NLRP3, ASC and Caspase-1 positive macrophages are positively correlated with the degree of optic nerve injury in POAG patients.
ABSTRACT
@#AIM: To investigate the effect of gene modification on the differentiation of bone marrow mesenchymal stem cells into neuron in treatment of optic nerve injury.<p>METHODS: Lentivirus carrying the rat ciliary neurotrophic factor(CNTF)coding sequence was transfected into bone marrow mesenchymal stem cells isolated from rat femur. Rats with optic nerve injury constructed by clamp optic nerve method were randomly divided into control group and study group. On the 4, 7, 10 and 13d after successful modeling, the transfused bone marrow were injected into the vitreous cavity of the study group. The control group was injected with the same amount of normal saline. On the 14<sup>th</sup> day after successful modeling, the light reflexes of the two groups of rats, the number of retinal ganglion cells and the expression of glial fibrillary acidic protein(GFAP)and Caspase-3 protein were observed.<p>RESULTS: The recovery rate of the study group was significantly higher than that of the control group(83% <i>vs</i> 25%, <i>P</i><0.05). The results showed that the retinal cells in the study group were relatively neat. A small amount of vacuoles were observed; the retinal cells in the control group were not well-structured, and obvious vacuoles were observed, and the number of cells was decreased. The results of Western blot showed that the expression level of GFAP and the expression level of Caspase-3 were higher than that of the rats in the study group.<p>CONCLUSION: Genetic modification induces bone marrow mesenchymal stem cells can effectively treat optic nerve injury in rats.
ABSTRACT
Objective To observe the effects of hyperbaric oxygen in the treatment of the rats with optic nerve crush. Methods In this study, 24 rats with traumatic optic nerve injury were recruited. The rats'left eyes were injured in the optic nerve and the right eyes as the controls were applied with sham-operation. The rats were divided into the treatment group and the control group in accordance with the random number table. The experimental group was treated with two-course hyperbaric oxygen one hour a day, 10 days a course. The control group breathed fresh air under standard atmospheric pressure. F-VEP was detected on day 3, 10, 20 during the experiment. Results In the control group, latency of F-VEP delayed (P＜0.05) and the amplitude of P100 decreased (P＜0.05) in the injured eye compared to the normal eye. In the experimental group, no obvious difference was found in the latency of F-VEP and the amplitude of P100 in the injured eye compared to the normal eye (P＞ 0.05) . The comparison of F-VEP data of the injured eyes showed that incubation period was in advance (P＜ 0.05) and amplitude increased (P＜0.05) in the experimental group. The comparison of F-VEP data tested at different time points was statistical significant. Conclusion The rat model of optic nerve injury was successful. Hyperbaric oxygen therapy showed no interference with the F-VEP data of the injured eye by causing no damage to the normal eye and was proved effective. Longer treatment provided better results.
ABSTRACT
The optic nerve belongs to the central nervous system (CNS).Because of the lack of neurotrophic factors in the microenvironment of the CNS and the presence of myelin and glial scar-related inhibitory molecules,and the inherent low renewal potentials of CNS neurons comparing to the peripheral nerve system,it is difficult to spontaneously regenerate the optic nerve after injury.Protecting damaged retinal ganglion cells (RGCs),supplementing neurotrophic factor,antagonizing axon regeneration inhibitory factor,and regulating the inherent regeneration potential of RGCs can effectively promote the regeneration and repair of optic nerve.Basic research has made important progress,including the restoration of visual function,but there are still a lot of unsolved problems in clinical translation of these achievements,so far there is no ideal method of treatment of optic nerve injury.Therefore,it is rather urgent to strengthen the cooperation between basic and clinical research,to promote the transformation of basic research to the clinical applications as soon as possible,which will change the unsatisfactory clinical application status.
ABSTRACT
Objective To explore the effect and potential mechanism of suppressors of cytokine signaling 3 (SOCS3) knockout on cell viability and apoptosis of retinal ganglion cells (RGCs) after optic nerve injury.Methods The optic nerve transection was used to construct optic nerve injury model of rats,and RGCs were isolated after optic nerve injury.The experimental animals were divided into optic nerve transection injury (ONT) group and sham-operation (Sham) group.The expression of SOCS3 in RGCs was detected by Western blot and RT-PCR in each group.Subsequently,SOCS3 siRNA was transfected into RGCs of Sham group and ONT group,and the experimental were further subdivided into blank control group,negative control group and SOCS3 silence groups.Cell viability was measured by CCK8 and MTr methods.Apoptosis was detected by Hoechst 33342 staining and flow cytometry.Furthermore,the mTOR siRNA and SOCS3 siRNA were co-transfected into RGCs,and cell viability and apoptosis were detected.Results The expression of SOCS3 was dramatically increased at 3 days after injury in the ONT group when compared with Sham group (P =0.049),and it showed an increased tendency gradually along with the extension of injury time.Compared with the blank control in the ONT group,SOCS3 silence markedly promoted cell viability [(49.47 ± 7.35) ％ vs.(73.24 ± 8.70) ％],reduced cell growth inhibition [(27.25 ±0.75)％ vs.(10.96 ± 1.07)％] and apoptosis [(23.06 ± 1.43)％ vs.(10.65 ± 1.77)％].The result of Hoechst 33342 staining indicated that SOCS3 silence ameliorated the cell apoptosis induced by ONT.In addition,SOCS3 silence significantly improved pS6 expression at 2 weeks after injury,and mTOR and SOCS3 co-silence reduced cell viability,increased cell growth inhibition and apoptosis compared with SOCS3 silence group after injury.Conclusion SOCS3 silence promotes injury-induced cell viability of RGCs and suppresses injury-induced apoptosis of RGCs via up-regulating mTOR activity in the later period of injury.
ABSTRACT
Background Traumatic optic neuropathy (TON) is an acute injury of the optic nerve secondary to trauma.As an important immune cell,microglia is involved in a variety of pathologic changes in central nervous system diseases and eye diseases.However,the role of microglia in the lesion development and neural restoration in TON is still unclear.Objective This study was to compare the differences of microglial activation between optic nerve axon and retina after optic nerve crush injury,including the morphological changes,number,and distribution of microglia.Methods Thirty-five SPF female Sprague-Dawley (SD) rats were numbered from 1 to 35 and randomized into normal control group,sham operation group and modeling 6-hour group,modeling 3-day group,modeling 7-day group,modeling 14-day group and modeling 30-day group according to the random number table.Optic nerve injury models were established by crushing optic nerve at retrobulbar 2 mm for 10 seconds.The same operation was carried out but not clamping optic nerve in the sham operation group,and normal control group without any treatment.The morphological changes,number and distribution of microglia in retina and optic nerve axon were assayed and compared by immunofluorescence staining with lectin-FITC fluorescence labeled antibody detection.The use and care of the experimental animals complied with ARVO.Results Microglia were displayed mainly in inner plexiform layer (IPL),and a few of microglia were in inner nuclear layer (INL) and ganglion cell layer (GCL),not any microglia were seen in outer nuclear layer (ONL) and outer plexiform layer (OPL) in the normal control group and sham operation group.Thining synapsis and secondary branches were seen with the dendroid in shape in normal control group.In the model groups,the microglia were more in GCL compared with sham operation group and showed amoeboid microglial cells.The number of microglia in retinas was 6.40 ± 1.52,7.20 ± 2.05,12.00 ± 3.54,14.00 ± 4.06,18.00±4.36,18.40 ± 3.13 and 10.80 ± 1.92 in the normal control group,sham operation group,modeling 6-hour group,modeling 3-day group,modeling 7-day group,modeling 14-day group and modeling 30-day group,respectively,and the microglia number were significantly increased in modeling 6-hour group,modeling 3-day group,modeling 7-day group,modeling 14-day group and modeling 30-day group in comparison with the normal control group,and in the modeling 30-day group,the microglial number in retinas was significantly reduced in comparison with the modeling 7-day group and modeling 14-day group (all at P＜0.05).The activited microglia in the retinas were nueh more in the modeling 3-day group,modeling 7-day group and modeling 14-day group than that in the sham operation group (P =0.024,0.009,0.023).In the optic nerve,the microglial cells were small in size and sparse in arrangement in the normal control group and sham operation group.The cells were enlarged with the amoeboid-like in shape in the model groups and distributed in injury area.The cell number was significantly higher in the modeling 6-hour group,modeling 3-day group,modeling 7-day group and modeling 14-day group than that in the normal control group (P=0.007,0.001,0.003,0.014).The cell number in modeling 30-day group was significnatly reduced in comparison with the modeling 3-day group,modeling 7-day group and modeling 14-day group (all at P＜0.05).The activated microglial number were significantly elevated in the modeling 6-hour group,modeling 3-day group,modeling 7-day group compared with the sham operation group (P =0.005,0.004,0.030),and the cell number in the modeling 30-day group was evidently lower than that in the modeling 3-day group (P =0.021,0.004).The cells of activated state in the optic nerve were significantly increased in modeling 6-hour group and modeling 14-day group.Conclusions Microglia are activated and keep increasing number in retina and optic nerve at a certain period after optic nerve injury,and these changes are earlier and more distinct in optic nerve axon than those in retina.