青光眼是一组以视盘萎缩凹陷、视野缺损以及视力下降为共同特征的视神经退行性疾病，也是世界首位不可逆性致盲眼病，导致患者生活质量降低、引起极大卫生经济负担。但其发病机制尚不明确，促进房水排出从而降低眼内压仍是目前减缓疾病进展的唯一治疗手段。房水排出的主要途径是经由小梁网进入Schlemm's管最后汇入巩膜外静脉，因此小梁网在调节房水排出以及平衡眼内压方面发挥重要作用。近年来，体内以及体外房水排出测量技术和小梁网成像技术不断突破，众多研究表明小梁网存在压力依赖的节律性搏动，在房水的脉冲式排出中起到关键作用，但在青光眼中这种搏动随疾病的进展减弱甚至消失。文章以小梁网的泵理论为核心，总结青光眼中房水排出的最新研究进展，并从恢复小梁网功能的角度出发探索可能有效的治疗策略，为青光眼的临床诊治提供新的思路。

Glaucoma, a group of optic nerve degenerative diseases, is characterized by papillary atrophy, visual field defects, and decreased vision. It is also the leading cause of irreversible blindness worldwide, significantly reducing patients’ the quality of life of patients and posing considerable health economic burdens. However, the pathogenesis of glaucoma remains unclear, and promoting aqueous humor outflow to reduce intraocular pressure is the only treatment option available to slow disease progression. The main pathway for aqueous humor outflow is through the trabecular meshwork into Schlemm's canal and finally into the episcleral veins, highlighting the crucial role of the trabecular meshwork in regulating aqueous humor outflow and maintaining intraocular pressure balance. In recent years, there have been notable breakthroughs in in vivo and in vitro aqueous humor outflow measurement techniques and trabecular meshwork imaging technologies.Many studies suggest that the trabecular meshwork exhibits pressure-dependent rhythmic pulsation, playing a crucial role in the pulse-like outflow of aqueous humor. Unfortunately, in glaucoma, this pulsation weakens or even disappears as the disease progresses. This article focuses on the trabecular meshwork's pump theory and summarizes the latest research progress in aqueous humor outflow in glaucoma, exploring potential effective therapeutic strategies aimed at restoring trabecular meshwork function. This provides new insights for the clinical diagnosis and treatment of glaucoma.

目的：研究雌二醇(estradiol，E2)和丙酸睾酮(testosterone propionate，TP)对兔泪腺上皮细胞凋亡及对MMP-9蛋白表达的影响，探讨雌二醇及丙酸睾酮对干眼的作用机制。方法：体外培养兔泪腺上皮细胞，分别给予雌二醇及丙酸睾酮处理，双氧水(H₂O₂)诱导细胞凋亡，流式细胞仪检测细胞凋亡和免疫细胞化学法检测细胞MMP-9蛋白表达。实验分4组：凋亡对照组(AC组)、雌二醇组(E2组)、丙酸睾酮组(TP组)和空白对照组(BC组)。AC组只给予H₂O₂诱导凋亡，E2组给予1×10^-5mol/L雌二醇处理，TP组给予丙酸睾酮处理，BC组未加药物干预及未加H2O2诱导凋亡。结果：经H₂O₂诱导细胞凋亡后，泪腺上皮细胞早期凋亡率和MMP-9蛋白表达累积光密度值与BC组相比，AC组、E2组及TP组均显著增加；同比AC组，E2组及TP组细胞凋亡率和MMP-9蛋白表达量降低；E2组凋亡率及蛋白表达量比TP组明显降低；其差异均具有统计学意义(P<0.01)。结论：雌二醇和丙酸睾酮对H₂O₂诱导兔泪腺上皮细胞凋亡有一定的抑制作用，同时泪腺上皮细胞中MMP-9表达含量也降低，提示雌二醇和丙酸睾酮抑制兔泪腺上皮细胞凋亡的作用机制可能与MMP-9有关。

Objective: To investigate the effects of estradiol (E2) and testosterone propionate (TP) on apoptosis and matrix metalloproteinase-9 (MMP-9) expression in rabbit lacrimal gland epithelial cells. Methods: The rabbit lacrimal gland epithelial cells were cultured in vitro. H₂O₂ was used to induce apoptosis in cultured lacrimal gland epithelial cells and then treated with E2 and TP respectively. Cell apoptosis was detected by flow cytometer (FCM) and MMP-9 expression was evaluated by immunocytochemistry. There were four groups: apoptosis control group (AC), estradiol group (E2), testosterone propionate group (TP) and blank control group (BC) respectively. The cells of group AC were administrated with H₂O₂ only, group E2 and group TP with 1×10^_5 mol/L E2 and TP respectively and group BC in treated. Statistical analysis were performed with one-way analysis of variance (ANOVA test)using SPSS 16.0, P<0.05 was considered statistically significant. Results: Compared with group BC, the early cells apoptosis rate and integrated optical density of MMP-9 expression of lacrimal gland in group AC, E2 and TP increased significantly after the cells were induced by H₂O₂; Compared with group AC, group E2 and TP reduced; group E2 were significantly lower than group TP; the differences were all statistically significant (P<0.01). Conclusion: E2 and TP had a certain inhibitory effect on rabbit lacrimal gland epithelial cells apoptosis induced by H₂O₂. Meanwhile, MMP-9 expression of the lacrimal gland cells was decreased. These results indicated that E2 and TP on the apoptosis inhibitory mechanism of lacrimal gland cells may be related with MMP-9. 

青光眼是一组以视盘萎缩凹陷、视野缺损以及视力下降为共同特征的视神经退行性疾病，也是世界首位不可逆性致盲眼病，导致患者生活质量降低、引起极大卫生经济负担。但其发病机制尚不明确，促进房水排出从而降低眼内压力仍是目前减缓疾病进展的唯一治疗手段。房水排出的主要途径是经由小梁网进入Schlemm’ s管最后汇入巩膜外静脉，因此小梁网在调节房水排出以及平衡眼内压力方面发挥重要作用。近年以来体内以及体外房水排出测量技术和小梁网成像技术不断突破，众多研究表明小梁网存在压力依赖的节律性搏动，在房水的脉冲式排出中起到关键作用，但在青光眼中这种搏动随疾病的进展减弱甚至消失。文章将以小梁网的泵理论为核心，总结青光眼中房水排出的最新研究进展，并从恢复小梁网功能的角度出发探索可能有效的治疗策略，为青光眼的临床诊治提供新的思路。

青光眼是一组以视盘萎缩凹陷、视野缺损以及视力下降为共同特征的视神经退行性疾病，也是世界首位不可逆性致盲眼病，导致患者生活质量降低、引起极大卫生经济负担。但其发病机制尚不明确，促进房水排出从而降低眼内压力仍是目前减缓疾病进展的唯一治疗手段。房水排出的主要途径是经由小梁网进入Schlemm’ s管最后汇入巩膜外静脉，因此小梁网在调节房水排出以及平衡眼内压力方面发挥重要作用。近年以来体内以及体外房水排出测量技术和小梁网成像技术不断突破，众多研究表明小梁网存在压力依赖的节律性搏动，在房水的脉冲式排出中起到关键作用，但在青光眼中这种搏动随疾病的进展减弱甚至消失。文章将以小梁网的泵理论为核心，总结青光眼中房水排出的最新研究进展，并从恢复小梁网功能的角度出发探索可能有效的治疗策略，为青光眼的临床诊治提供新的思路。

       “锌”在青光眼研究舞台上正扮演着越来越重要的角色。糖皮质激素，作为人体内重要的激素之一，其对锌的调控已在诸多系统中被证实。研究发现，在糖皮质激素的影响下，小梁网中的锌离子转运受阻，导致细胞外基质降解失衡，从而干扰小梁网正常流出道功能，加重青光眼的病情。而视神经损伤后，锌离子在神经突触间的异常传递、不平衡分布与胞内异常累积影响视网膜神经节细胞存活和轴突的再生能力，进而损害视功能，可能成为青光眼视神经损伤发病及进展的关键因素。这些研究进展为视神经保护策略提供了新的视角，“锌”作为治疗靶点的潜力正在被逐步挖掘，通过调节锌水平来干预青光眼病理进程成为可能治疗手段。
       本期封面中将汉字“锌”设计为飞天舞者，其超越时空的永恒美感，呼应了“锌”在青光眼研究中突破传统、开辟新程的角色。轻盈与自由的飞天舞者，象征着“锌”在细胞内外穿梭，精妙调控生理功能，维系细胞的和谐与平衡，为青光眼患者带来新的治疗希望。

       “锌”在青光眼研究舞台上正扮演着越来越重要的角色。糖皮质激素，作为人体内重要的激素之一，其对锌的调控已在诸多系统中被证实。研究发现，在糖皮质激素的影响下，小梁网中的锌离子转运受阻，导致细胞外基质降解失衡，从而干扰小梁网正常流出道功能，加重青光眼的病情。而视神经损伤后，锌离子在神经突触间的异常传递、不平衡分布与胞内异常累积影响视网膜神经节细胞存活和轴突的再生能力，进而损害视功能，可能成为青光眼视神经损伤发病及进展的关键因素。这些研究进展为视神经保护策略提供了新的视角，“锌”作为治疗靶点的潜力正在被逐步挖掘，通过调节锌水平来干预青光眼病理进程成为可能治疗手段。

       本期封面中将汉字“锌”设计为飞天舞者，其超越时空的永恒美感，呼应了“锌”在青光眼研究中突破传统、开辟新程的角色。轻盈与自由的飞天舞者，象征着“锌”在细胞内外穿梭，精妙调控生理功能，维系细胞的和谐与平衡，为青光眼患者带来新的治疗希望。

糖皮质激素(glucocorticoid, GC)由于其抗炎特性被广泛用于治疗眼部炎症，而G C诱导性青光眼(glucocorticoid-induced glaucoma, GIG) 作为一种常见并发症，其发病机制长期受到关注。文章综述了锌在GIG中的关键作用及其调控机制，揭示了锌在青光眼发病机制中的重要角色。锌作为人体中含量第二丰富的过渡金属，对蛋白质结构、酶催化和细胞信号调节至关重要。GC对锌分布的调控作用在不同组织和细胞类型中表现出复杂性，影响锌的摄取和释放，进而参与青光眼的病理过程。锌通过影响小梁网细胞外基质(extracellular matrix, ECM)的降解和重塑，以及视网膜神经节细胞的存活和轴突再生，在GIG的发病机制中发挥着复杂的作用。文章同时介绍了体内锌调控的现有途径，包括补充锌和减少锌的策略，提供了潜在的治疗途径。未来的研究应深入探索锌在青光眼中的作用机制以及与GC的相互作用，评估锌补充或螯合在青光眼治疗中的安全性和有效性，以及开发新型锌递送和螯合系统，有助于全面揭示锌在青光眼中的作用及治疗潜力，以实现更加精准的防治方案，改善患者预后。

Glucocorticoid (GC) is widely used in the treatment of ocular inflammation for its anti-inflammatory propery. However, glucocorticoid-induced glaucoma (GIG) is a common complication, and its pathogenesis has been extensively studied. This review summarizes the crucial role of zinc in GIG and its regulatory mechanisms, highlighting zinc's significant involvement in the pathogenesis of glaucoma. Zinc, the second most abundant transition metal in the human body, is essential for protein structure, enzyme catalysis, and cell signaling regulation. The effects of GC on zinc distribution vary across different tissues and cell types, affecting zinc uptake and release, which may contribute to the pathological processes of glaucoma. Zinc influences the degradation and remodeling of the trabecular meshwork extracellular matrix and the survival and axonal regeneration of retinal ganglion cells, playing complex roles in the pathogenesis of GIG. We discuss available strategies for regulating zinc in vivo, including zinc supplementation and reduction strategies, providing potential therapeutic approaches. Future research should explore the mechanisms of zinc's role in glaucoma and its interaction with glucocorticoids, evaluate the safety and efficacy of zinc supplementation or chelation in glaucoma treatment, and develop novel zinc delivery and chelation systems. These efforts will help fully elucidate the role of zinc in glaucoma and its therapeutic potential, enabling more precise prevention and treatment strategies to improve patient outcomes.

干眼是以泪膜稳态丢失及伴随眼部不适症状为特征的最常见眼表疾病，泪膜不稳定、泪液高渗透性、眼表炎症及感觉神经异常为其主要病因。地夸磷索钠是一种P2Y2受体激动剂，能刺激黏蛋白及泪液分泌，其独特的作用机制为干眼的治疗开辟了新的方向，本文就地夸磷索钠近年的临床及基础研究进展作一综述。

Dry eye is one of the most common ocular surface diseases. It is characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and tear hyperosmolarity, ocular surface inflammation, and neurosensory abnormalities play major etiological roles. Diquafosol tetrasodium is a purinergic P2Y2 receptor agonist that promotes mucin and aqueous tear secretion. The unique pharmacological mechanism of diquafosol tetrasodium opens up a new direction for the medical therapies of dry eye. This article reviews the clinical therapeutic effect and research progress of diquafosol tetrasodium for the past few years.