目的：通过真实的临床病例，分析青光眼与非青光眼性视神经病变的不同表现，提高疾病的鉴别诊断能力。方法：采用病例研究与文献回顾方法，记录3例易误诊为正常眼压性青光眼（normal tension glaucoma, NTG）的神经眼科病例，通过视力、眼压、瞳孔对光反应、视盘形态、RNFL厚度、视野损害等特点，抽丝剥茧，得出诊断。结果：病例1视野呈弓形缺损，但视盘凹陷不深，且对侧眼“视盘拥挤”，随访期间发生急性前部缺血性视神经改变(anterior ischaemic optic neuropathy, AION)，最终确诊“AION遗留视神经萎缩”。病例2视力下降、视野缺损与视神经结构损害不相符，经完善MRI确诊为“左侧视神经鞘膜瘤”。病例3青年男性，中心视力下降，视盘凹陷不深，根据DNA结果确诊Leber遗传性视神经病变（Leber hereditary optic neuropathy, LHON）。结论：通过几个典型的神经眼科病例，掌握AION、视神经鞘膜瘤、LHON的结构和功能损害特征，如视盘凹陷不深、中心视力下降、视神经结构损害与视功能不相符，与NTG相鉴别。
Objective: To analyze the differentiating manifestations of glaucomatous and non-glaucomatous optic neuropathies using real clinical cases and to enhance the ability to make differential diagnosis. Methods: By using case study and literature review methods, we recorded three neuro-ophthalmic cases that were prone to being misdiagnosed as normal tension glaucoma (NTG). The diagnosis was established by extracting features related to visual acuity, intraocular pressure, pupillary light reflex, optic disc morphology, retinal nerve fiber layer (RNFL) thickness and visual field damage. Results: Case 1 presented with arcuate visual field defects, shallow optic disc cupping, and contralateral crowded discs. During follow-up, the patient subsequently developed acute anterior ischemic optic neuropathy (AION), and the final diagnosis confirmed was confirmed as optic atrophy secondary to AION. Case 2 exhibited a disproportionate visual acuity decline and visual field defects that were inconsistent with glaucomatous structural damage. MRI confirmed the diagnosis of left optic nerve sheath meningioma. Case 3 involved a young male who presented with central vision loss and shallow optic disc cupping. Genetic testing confirmed Leber's hereditary optic neuropathy (LHON). Conclusions: Through these representative neuro-ophthalmology cases, we illustrate the characteristic patterns of structural and functional damage associated with AION, optic nerve sheath meningioma, and LHON, such as shallow optic disc cupping, central vision loss, and inconsistency between optic nerve structural damage and visual function. These findings highlight the key differentiating features of these conditions from NTG.
目的：通过在人小梁网细胞(human trabecular meshwork cell，HTMC)中过表达沉默信息调节因子2相关酶1(silent information regulator 1，SIRT1)，探讨SIRT1对氧化应激下HTMC功能的影响。方法：将SIRT1过表达慢病毒和GFP阴性对照慢病毒按照最佳(multiplicity of infection，MOI)分别转染入HTMC，并用实时定量PCR法对SIRT1是否在细胞中过表达进行验证。实验分为以下4组：正常组、H2O2组、H2O2+Lv-SIRT1-OE(过表达)组、H2O2+Lv-GFP组，分别采用Transwell法和CCK8法检测氧化应激下HTMC的迁移能力和活性。两组间比较采用独立样本t检验。结果：在正常组、H2O2组、H2O2+Lv-SIRT1-OE组、H2O2+Lv-GFP组这4组中，Transwel l实验结果分别为436±73、254±25、510±51、327±46，H2O2+Lv-SIRT1-OE组分别与H2O2组和H2O2+Lv-GFP组差异均有统计学意义(P<0.01)。CCK8法结果显示，H2O2+Lv-SIRT1-OE组分别与H2O2组和H2O2+Lv-GFP组相比差异均有统计学意义(P<0.01)。H2O2+Lv-SIRT1-OE组分别与H2O2组和阴性对照组(H2O2+Lv-GFP)相比，Bax表达水平明显下降，Bcl-2表达水平明显提高，差异均有统计学意义(P<0.01)。ROS活性氧测定显示H2O2+Lv-SIRT1-OE组比H2O2组的细胞活性氧水平显著降低(P<0.05)。结论：在HTMC中过表达SIRT1能有效降低氧化应激对HTMC迁移能力和活性的影响，从而对HTMC起到一定的保护作用，为后续研究SIRT1保护氧化应激下HTMC的调控机制打下基础。
Objective: To explore the effect of Silent Information Regulator 1 (SIRT1) on cell function of human trabecular meshwork cell (HTMC) under oxidative stress by overexpressing SIRT1 in HTMC. Methods: This is an experiment research. HTMCs were transfected with SIRT1-ovexpressed lentivirus and GFP-negative control lentivirus (Lv-GFP) at the optimal multiplicity of infection (MOI). Real-time quantitative PCR was used to verify whether SIRT1 was overexpressed in HTMC. The following experiments were divided into four groups: normal control group, H2O2 group,H2O2+Lv-SIRT1-OE group, H2O2+Lv-GFP group. Cell migration was detected by transwell assay. Cell viability was detected by CCK8 assay. Student’s t-test was used for two groups. P<0.05 was set as statistical signifificance. Results: The number of migration per well of normal control group, H2O2 group, H2O2+Lv-SIRT1-OE group, H2O2+Lv-GFP group were 436±73,254±25, 510±51, 327±46, respectively. Compared with H2O2 group and H2O2+Lv-GFP group, transwell assay demonstrated that the number of migrations per well of H2O2+Lv-SIRT1-OE group significantly increased (P<0.01). Likewise, CCK8 assay indicated that cell viability of H2O2+Lv-SIRT1-OE group was higher than both of H2O2 group and H2O2+Lv-GFP group (P<0.01). Compared with H2O2+Lv-SIRT1-OE group and negative control group (H2O2+Lv-GFP), the expression level of Bax decreased significantly,and the expression level of Bcl-2 increased significantly (P<0.01). ROS assay showed that the ROS level in H2O2+Lv-SIRT1-OE group was significantly lower than that in H2O2 group (P<0.05). Conclusion:SIRT1 overexpressed in HTMC can effectively reduce the effect of oxidative stress on migration ability and proliferation activity of HTMC, which lays a foundation for further study on the regulatory mechanism of SIRT1 protecting HTMC under oxidative stress.
目的：通过在人小梁网细胞(human trabecular meshwork cell，HTMC)中过表达沉默信息调节因子2相关酶1(silent information regulator 1，SIRT1)，探讨SIRT1对氧化应激下HTMC功能的影响。方法：将SIRT1过表达慢病毒和GFP阴性对照慢病毒按照最佳(multiplicity of infection，MOI)分别转染入HTMC，并用实时定量PCR法对SIRT1是否在细胞中过表达进行验证。实验分为以下4组：正常组、H2O2组、H2O2+Lv-SIRT1-OE(过表达)组、H2O2+Lv-GFP组，分别采用Transwell法和CCK8法检测氧化应激下HTMC的迁移能力和活性。两组间比较采用独立样本t检验。结果：在正常组、H2O2组、H2O2+Lv-SIRT1-OE组、H2O2+Lv-GFP组这4组中，Transwell实验结果分别为436±73、254±25、510±51、327±46，H2O2+Lv-SIRT1-OE组分别与H2O2组和H2O2+Lv-GFP组差异均有统计学意义(P<0.01)。CCK8法结果显示，H2O2+Lv-SIRT1-OE组分别与H2O2组和H2O2+Lv-GFP组相比差异均有统计学意义(P<0.01)。H2O2+Lv-SIRT1-OE组分别与H2O2组和阴性对照组(H2O2+Lv-GFP)相比，Bax表达水平明显下降，Bcl-2表达水平明显提高，差异均有统计学意义(P<0.01)。ROS活性氧测定显示H2O2+Lv-SIRT1-OE组比H2O2组的细胞活性氧水平显著降低(P<0.05)。结论：在HTMC中过表达SIRT1能有效降低氧化应激对HTMC迁移能力和活性的影响，从而对HTMC起到一定的保护作用，为后续研究SIRT1保护氧化应激下HTMC的调控机制打下基础。
Objective: To explore the effect of Silent Information Regulator 1 (SIRT1) on cell function of human trabecular meshwork cell (HTMC) under oxidative stress by overexpressing SIRT1 in HTMC. Methods: This is an experiment research. HTMCs were transfected with SIRT1-ovexpressed lentivirus and GFP-negative control lentivirus (Lv-GFP) at the optimal multiplicity of infection (MOI). Real-time quantitative PCR was used to verify whether SIRT1 was overexpressed in HTMC. The following experiments were divided into four groups: normal control group, H2O2 group, H2O2+Lv-SIRT1-OE group, H2O2+Lv-GFP group. Cell migration was detected by transwell assay. Cell viability was detected by CCK8 assay. Student’s t-test was used for two groups. P<0.05 was set as statistical signi?cance. Results: The number of migration per well of normal control group, H2O2 group, H2O2+Lv-SIRT1-OE group, H2O2+Lv-GFP group were 436±73, 254±25, 510±51, 327±46, respectively. Compared with H2O2 group and H2O2+Lv-GFP group, transwell assay demonstrated that the number of migrations per well of H2O2+Lv-SIRT1-OE group significantly increased (P<0.01). Likewise, CCK8 assay indicated that cell viability of H2O2+Lv-SIRT1-OE group was higher than both of H2O2 group and H2O2+Lv-GFP group (P<0.01). Compared with H2O2+Lv-SIRT1-OE group and negative control group (H2O2+Lv-GFP), the expression level of Bax decreased significantly, and the expression level of Bcl-2 increased significantly (P<0.01). ROS assay showed that the ROS level in H2O2+Lv-SIRT1-OE group was significantly lower than that in H2O2 group (P<0.05). Conclusion: SIRT1 overexpressed in HTMC can effectively reduce the effect of oxidative stress on migration ability and proliferation activity of HTMC, which lays a foundation for further study on the regulatory mechanism of SIRT1 protecting HTMC under oxidative stress.
