Experimental eye research最新文献

Rapid anterior segment and divergent corneal shape remodeling drive astigmatic compensation in the chick model 快速前段和发散性角膜形状重塑驱动鸡模型的散光代偿

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-13 DOI: 10.1016/j.exer.2026.110861

Yuanyuan Liang , Tsz Wing Leung , Patience Ansomah Ayerakwah , Byung Soo Kang , Chea-su Kee

This study investigated early temporal dynamics of ocular compensation to imposed astigmatic blur, specifically anterior segment alterations in a chick model. Fifty-four chickens were equally randomized to treatment or control groups at post-hatching day 5 (baseline, T0). Crossed-cylindrical lens (+4.00 DS/−8.00 DC) was used to induce astigmatic blur on the right eye for two weeks: With-the-rule (WTR, axis 90°) and Against-the-rule (ATR, axis 180°) astigmatism. Ocular axial dimensions and objective refraction were measured daily for the first four days (T0-T3), and at one (T7) and two weeks (T14). Corneal topography was measured at T3, T7 and T14. Our results showed that chicks treated with crossed-cylindrical lenses developed significantly higher refractive astigmatism compared to the control group (all p < 0.01), plateauing within two days. Corneal astigmatism diverged over two weeks, increasing in the WTR group but decreasing in the ATR groups, while internal astigmatism showed opposite trends. Critically, anterior segment changes emerged by T3: the ATR group exhibited a significantly deeper anterior chamber (T3: p = 0.034), and both treatment groups showed significantly thinner crystalline lenses (ATR: T2, p = 0.008; T3, p = 0.007; WTR: T3, p = 0.043) compared to controls. These changes persisted throughout the treatment. To conclude, refractive astigmatism compensated rapidly (plateauing within two days) in response to astigmatic blur, while corneal astigmatism exhibited divergent changes over two weeks. The persistent anterior segment alterations—lens thinning and anterior chamber deepening—demonstrate a key compensatory role for anterior ocular structures beyond corneal plasticity alone.

本研究调查了早期的时间动态眼代偿强加的散光模糊，特别是前段的变化，在一个小鸡模型。54只鸡在孵化后第5天（基线，T0）随机分为处理组和对照组。采用交叉柱状晶状体（+4.00 DS/−8.00 DC）诱导右眼散光模糊2周：顺行（WTR，轴90°）和反行（ATR，轴180°）散光。前4天（T0-T3）、第1周（T7）和第2周（T14）每天测量眼轴尺寸和物镜屈光度。在T3、T7、T14时测量角膜地形图。结果表明，与对照组相比，经交叉柱面透镜处理的雏鸡的屈光散光明显增加（p < 0.01），并在2天内趋于稳定。角膜散光在两周内出现分化，WTR组增加，ATR组减少，而内部散光则呈现相反的趋势。重要的是，T3出现了前段的改变：与对照组相比，ATR组的前房明显加深（T3: p = 0.034），两个治疗组的晶状体明显变薄（ATR: T2, p = 0.008; T3, p = 0.007; WTR: T3, p = 0.043）。这些变化在整个治疗过程中持续存在。综上所述，屈光散光对散光模糊的反应补偿迅速（2天内稳定），而角膜散光在两周内表现出不同的变化。持续的前段改变——晶状体变薄和前房加深——表明除了角膜可塑性外，前眼结构还具有重要的代偿作用。

{"title":"Rapid anterior segment and divergent corneal shape remodeling drive astigmatic compensation in the chick model","authors":"Yuanyuan Liang , Tsz Wing Leung , Patience Ansomah Ayerakwah , Byung Soo Kang , Chea-su Kee","doi":"10.1016/j.exer.2026.110861","DOIUrl":"10.1016/j.exer.2026.110861","url":null,"abstract":"<div><div>This study investigated early temporal dynamics of ocular compensation to imposed astigmatic blur, specifically anterior segment alterations in a chick model. Fifty-four chickens were equally randomized to treatment or control groups at post-hatching day 5 (baseline, T0). Crossed-cylindrical lens (+4.00 DS/−8.00 DC) was used to induce astigmatic blur on the right eye for two weeks: With-the-rule (WTR, axis 90°) and Against-the-rule (ATR, axis 180°) astigmatism. Ocular axial dimensions and objective refraction were measured daily for the first four days (T0-T3), and at one (T7) and two weeks (T14). Corneal topography was measured at T3, T7 and T14. Our results showed that chicks treated with crossed-cylindrical lenses developed significantly higher refractive astigmatism compared to the control group (all <em>p</em> < 0.01), plateauing within two days. Corneal astigmatism diverged over two weeks, increasing in the WTR group but decreasing in the ATR groups, while internal astigmatism showed opposite trends. Critically, anterior segment changes emerged by T3: the ATR group exhibited a significantly deeper anterior chamber (T3: <em>p</em> = 0.034), and both treatment groups showed significantly thinner crystalline lenses (ATR: T2, <em>p</em> = 0.008; T3, <em>p</em> = 0.007; WTR: T3, <em>p</em> = 0.043) compared to controls. These changes persisted throughout the treatment. To conclude, refractive astigmatism compensated rapidly (plateauing within two days) in response to astigmatic blur, while corneal astigmatism exhibited divergent changes over two weeks. The persistent anterior segment alterations—lens thinning and anterior chamber deepening—demonstrate a key compensatory role for anterior ocular structures beyond corneal plasticity alone.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110861"},"PeriodicalIF":2.7,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Betanin protects against diabetic retinal damage via the inhibition of NF-κB/NLRP3/VEGF axis: Insights from network pharmacology and experimental studies 甜菜素通过抑制NF-κB/NLRP3/VEGF轴保护糖尿病视网膜损伤：网络药理学和实验研究的见解

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-13 DOI: 10.1016/j.exer.2026.110863

Sawsan Zaitone , Nema Soliman , Amany M. Shalaby , Ahmed A. Abdelgbar , Mohamed A.K. Saleh , Ahmed A. Farrag , Abdelhakeem A. Elaskary , Esam Ghanem Abu El Wafa , Amira H. Eltrawy , Fatma Azzahraa Hisham , Sozan M. Abdelkhalig , Rehab M. El-Sayed

Diabetic retinopathy (DIR) is a predominant diabetic microvascular complication that may cause vision loss. Retinal inflammation and angiogenesis contribute largely to the neuronal degeneration in DIR. The current study is aiming to test the effect of oral betanin doses in protection from DIR in rats along with a network pharmacology study to investigate an assumption that betanin may inhibit nuclear factor-κ B (NF-κB). Three rat groups were assigned as vehicle, DIR, and DIR + Betanin 100 mg/kg. Molecular docking indicated the possible binding between betanin and NF-κB while the bioinformatic study highlighted a relation between this possible inhibition and suppression of NOD-like receptor pyrin domain-containing protein 3/vascular endothelial growth factor (NLRP3/VEGF) axis. The rat experimental study validated this assumption and indicated a protective effect for betanin on rat retinas as shown by routine hematoxylin and eosin staining (retinal thickness and ganglion cell count) and periodic acid-Schiff staining that was mediated through mitigating expression/protein level for of NF-κB, NLRP3, TNF-α, IL-6 and VEGF proteins. Immunohistochemistry showed that betanin was able to suppress retinal content of the glial fibrillary acidic protein (GFAP). In conclusion, the current study indicated that betanin was a good candidate for DIR in rats through suppression of the inflammatory cascade and may be suggested for diabetic patients if appropriated clinical studies will be available.

糖尿病视网膜病变（DIR）是一种主要的糖尿病微血管并发症，可导致视力丧失。视网膜炎症和血管生成在很大程度上促进了视网膜病变的神经元变性。本研究旨在检测口服甜菜素对大鼠DIR的保护作用，并通过网络药理学研究来探讨甜菜素可能抑制核因子-κB （NF-κB）的假设。3组大鼠分别作为对照、DIR和DIR +甜菜素100 mg/kg。分子对接提示甜菜素可能与NF-κB结合，生物信息学研究强调了这种可能的抑制与nod样受体pyrin结构域蛋白3/血管内皮生长因子（NLRP3/VEGF）轴的抑制之间的关系。大鼠实验研究证实了这一假设，并通过常规苏木精和伊红染色（视网膜厚度和神经节细胞计数）和周期性酸希夫染色显示了甜菜素对大鼠视网膜的保护作用，这是通过降低NF-κB、NLRP3、TNF-α、IL-6和VEGF蛋白的表达/蛋白水平介导的。免疫组织化学表明，甜菜素能够抑制视网膜胶质原纤维酸性蛋白（GFAP）的含量。总之，目前的研究表明，甜菜素通过抑制炎症级联，是大鼠DIR的良好候选者，如果有适当的临床研究，可能会建议用于糖尿病患者。

{"title":"Betanin protects against diabetic retinal damage via the inhibition of NF-κB/NLRP3/VEGF axis: Insights from network pharmacology and experimental studies","authors":"Sawsan Zaitone , Nema Soliman , Amany M. Shalaby , Ahmed A. Abdelgbar , Mohamed A.K. Saleh , Ahmed A. Farrag , Abdelhakeem A. Elaskary , Esam Ghanem Abu El Wafa , Amira H. Eltrawy , Fatma Azzahraa Hisham , Sozan M. Abdelkhalig , Rehab M. El-Sayed","doi":"10.1016/j.exer.2026.110863","DOIUrl":"10.1016/j.exer.2026.110863","url":null,"abstract":"<div><div>Diabetic retinopathy (DIR) is a predominant diabetic microvascular complication that may cause vision loss. Retinal inflammation and angiogenesis contribute largely to the neuronal degeneration in DIR. The current study is aiming to test the effect of oral betanin doses in protection from DIR in rats along with a network pharmacology study to investigate an assumption that betanin may inhibit nuclear factor-κ B (NF-κB). Three rat groups were assigned as vehicle, DIR, and DIR + Betanin 100 mg/kg. Molecular docking indicated the possible binding between betanin and NF-κB while the bioinformatic study highlighted a relation between this possible inhibition and suppression of NOD-like receptor pyrin domain-containing protein 3/vascular endothelial growth factor (NLRP3/VEGF) axis. The rat experimental study validated this assumption and indicated a protective effect for betanin on rat retinas as shown by routine hematoxylin and eosin staining (retinal thickness and ganglion cell count) and periodic acid-Schiff staining that was mediated through mitigating expression/protein level for of NF-κB, NLRP3, TNF-α, IL-6 and VEGF proteins. Immunohistochemistry showed that betanin was able to suppress retinal content of the glial fibrillary acidic protein (GFAP). In conclusion, the current study indicated that betanin was a good candidate for DIR in rats through suppression of the inflammatory cascade and may be suggested for diabetic patients if appropriated clinical studies will be available.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110863"},"PeriodicalIF":2.7,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ocular rigidity in eyes with experimental myopia 实验性近视眼的眼强直

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-12 DOI: 10.1016/j.exer.2026.110859

Suharsha Paidimarri, Nimesh B. Patel, Krista M. Beach, Jacinth J. Priscilla, Raman P. Sah, Manoj K. Manoharan, Rakesh Maldoddi, Lisa A. Ostrin

Purpose

To evaluate ocular rigidity in experimentally induced myopic eyes compared to contralateral control eyes in young rhesus monkeys.

Methods

Eight rhesus monkeys (Macaca mulatta) were reared with monocular form-deprivation from 24 days to 150 days of age. Refraction, axial length, and intraocular pressure (IOP) were measured biweekly. After 150 days, ocular rigidity was assessed in both eyes via anterior chamber cannulation, in which controlled changes in anterior chamber volume were used to calculate the coefficient of ocular rigidity using Friedenwald's equation. Paired t-tests were used to compare form-deprived and control eyes, and Pearson's correlations were used to examine relationships between ocular rigidity, refraction, and axial length.

Results

After 150 days, form-deprived eyes were significantly less hyperopic (+0.41 ± 3.89 D vs. +3.10 ± 3.01 D, P = 0.03) and had longer axial lengths (16.54 ± 0.81 mm vs. 15.90 ± 0.76 mm, P = 0.01) than control eyes. Mean ocular rigidity coefficients were not significantly different between form-deprived and control eyes (0.054 ± 0.008 vs. 0.050 ± 0.010 μL⁻¹ P = 0.06).

Discussion

Form-deprivation myopia in young rhesus monkeys produced significant axial elongation and myopic shifts but did not significantly alter the coefficient of ocular rigidity. Although ocular rigidity showed a decreasing trend with increasing eye size, the limited range of axial lengths may have constrained statistical power to detect a small-to-moderate difference in the ocular rigidity coefficients between treated and control eyes. This work establishes direct in vivo assessment of ocular rigidity in a primate model, laying the groundwork for future approaches to examine ocular biomechanics in myopia.

目的评价实验性近视眼与对侧对照眼的眼强直。方法选取猕猴8只，在24 ~ 150日龄进行单眼形态剥夺饲养。每两周测量一次屈光、眼轴长度和眼内压。150天后，通过前房插管评估双眼眼僵硬度，其中前房容积的控制变化利用Friedenwald方程计算眼僵硬系数。配对t检验用于比较失形眼和对照眼，Pearson相关性用于检验眼强直、屈光度和眼轴长度之间的关系。结果150 D后，失形眼的远视程度显著低于对照组（+0.41±3.89 D vs +3.10±3.01 D, P = 0.03），眼轴长度显著高于对照组（16.54±0.81 mm vs 15.90±0.76 mm, P = 0.01）。失形眼和对照眼的平均眼刚度系数无显著差异（0.054±0.008 vs. 0.050±0.010 μL−1 P = 0.06）。年幼恒河猴形体剥夺性近视产生显著的眼轴伸长和近视眼移位，但对眼强直系数无显著影响。虽然眼硬度随眼睛尺寸的增大而下降，但轴向长度的有限范围可能限制了检测治疗眼和对照眼之间眼硬度系数的小到中等差异的统计能力。本研究在灵长类动物模型中建立了眼刚性的直接体内评估，为未来研究近视的眼生物力学奠定了基础。

{"title":"Ocular rigidity in eyes with experimental myopia","authors":"Suharsha Paidimarri, Nimesh B. Patel, Krista M. Beach, Jacinth J. Priscilla, Raman P. Sah, Manoj K. Manoharan, Rakesh Maldoddi, Lisa A. Ostrin","doi":"10.1016/j.exer.2026.110859","DOIUrl":"10.1016/j.exer.2026.110859","url":null,"abstract":"<div><h3>Purpose</h3><div>To evaluate ocular rigidity in experimentally induced myopic eyes compared to contralateral control eyes in young rhesus monkeys.</div></div><div><h3>Methods</h3><div>Eight rhesus monkeys (<em>Macaca mulatta</em>) were reared with monocular form-deprivation from 24 days to 150 days of age. Refraction, axial length, and intraocular pressure (IOP) were measured biweekly. After 150 days, ocular rigidity was assessed in both eyes via anterior chamber cannulation, in which controlled changes in anterior chamber volume were used to calculate the coefficient of ocular rigidity using Friedenwald's equation. Paired t-tests were used to compare form-deprived and control eyes, and Pearson's correlations were used to examine relationships between ocular rigidity, refraction, and axial length.</div></div><div><h3>Results</h3><div>After 150 days, form-deprived eyes were significantly less hyperopic (+0.41 ± 3.89 D vs. +3.10 ± 3.01 D, P = 0.03) and had longer axial lengths (16.54 ± 0.81 mm vs. 15.90 ± 0.76 mm, P = 0.01) than control eyes. Mean ocular rigidity coefficients were not significantly different between form-deprived and control eyes (0.054 ± 0.008 vs. 0.050 ± 0.010 μL<sup>−1</sup> P = 0.06).</div></div><div><h3>Discussion</h3><div>Form-deprivation myopia in young rhesus monkeys produced significant axial elongation and myopic shifts but did not significantly alter the coefficient of ocular rigidity. Although ocular rigidity showed a decreasing trend with increasing eye size, the limited range of axial lengths may have constrained statistical power to detect a small-to-moderate difference in the ocular rigidity coefficients between treated and control eyes. This work establishes direct <em>in vivo</em> assessment of ocular rigidity in a primate model, laying the groundwork for future approaches to examine ocular biomechanics in myopia.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110859"},"PeriodicalIF":2.7,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Non-neuronal cell microenvironment control retinal vascular remodeling by CST3 in the oxygen-induced retinopathy in mice. 非神经元细胞微环境通过CST3调控氧致视网膜病变小鼠视网膜血管重构。

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-12 DOI: 10.1016/j.exer.2026.110860

Ming-Yan Du, Chao Qu, Tu-Jing Zhao, Yan-Hui Deng, Lin Ye, Hua-Ping Tian, Run-Ze Li, Zheng Li, Hao-Jue Xu, Jie Li, Liang Zhou, Yi Shi, Lu-Lin Huang

Retinopathy of prematurity (ROP) remains the leading cause of blindness in premature infants owing to abnormal retinal blood vessels development,but molecular mechanisms are still not fully elucidated. Oxygen-induced retinopathy (OIR) mouse is the extensively used angiogenesis model for the study of ROP pathogenesis. In this study, we investigated five cell types that composed the microenvironment of retinal vessels in OIR mice by single-cell RNA sequencing (scRNA-seq) and revealed a complex and time-dependent regulation of vascular arrest and angiogenesis in the OIR microenvironment. Importantly, we also observe that Müller glia exhibit robust expression of CST3 (cysteine protease inhibitor cystatin C) during the early phase of hypoxic adaptation, leading to capillary morphogenesis in the hyaloid, disrupting physiological vascular patterning and contributing to OIR development. Altogether, our study reveals pivotal roles of the retinal microenvironment in both normal vascularization and ROP progression,suggesting that CST3 is a potential therapeutic target for ROP.

早产儿视网膜病变（ROP）是导致早产儿失明的主要原因，主要是由于视网膜血管发育异常，但其分子机制尚未完全阐明。氧诱导视网膜病变（OIR）小鼠是目前广泛应用于ROP发病机制研究的血管生成模型。在这项研究中，我们通过单细胞RNA测序（scRNA-seq）研究了构成OIR小鼠视网膜血管微环境的五种细胞类型，揭示了OIR微环境中血管骤停和血管生成的复杂和时间依赖性调控。重要的是，我们还观察到，在低氧适应的早期阶段，m ller胶质细胞表现出CST3（半胱氨酸蛋白酶抑制剂胱抑素C）的强烈表达，导致玻璃体中的毛细血管形态发生，破坏生理血管模式并促进OIR的发展。总之，我们的研究揭示了视网膜微环境在正常血管化和ROP进展中的关键作用，表明CST3是ROP的潜在治疗靶点。

{"title":"Non-neuronal cell microenvironment control retinal vascular remodeling by CST3 in the oxygen-induced retinopathy in mice.","authors":"Ming-Yan Du, Chao Qu, Tu-Jing Zhao, Yan-Hui Deng, Lin Ye, Hua-Ping Tian, Run-Ze Li, Zheng Li, Hao-Jue Xu, Jie Li, Liang Zhou, Yi Shi, Lu-Lin Huang","doi":"10.1016/j.exer.2026.110860","DOIUrl":"https://doi.org/10.1016/j.exer.2026.110860","url":null,"abstract":"<p><p>Retinopathy of prematurity (ROP) remains the leading cause of blindness in premature infants owing to abnormal retinal blood vessels development,but molecular mechanisms are still not fully elucidated. Oxygen-induced retinopathy (OIR) mouse is the extensively used angiogenesis model for the study of ROP pathogenesis. In this study, we investigated five cell types that composed the microenvironment of retinal vessels in OIR mice by single-cell RNA sequencing (scRNA-seq) and revealed a complex and time-dependent regulation of vascular arrest and angiogenesis in the OIR microenvironment. Importantly, we also observe that Müller glia exhibit robust expression of CST3 (cysteine protease inhibitor cystatin C) during the early phase of hypoxic adaptation, leading to capillary morphogenesis in the hyaloid, disrupting physiological vascular patterning and contributing to OIR development. Altogether, our study reveals pivotal roles of the retinal microenvironment in both normal vascularization and ROP progression,suggesting that CST3 is a potential therapeutic target for ROP.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110860"},"PeriodicalIF":2.7,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Calpain-1 C2L domain peptide protects retinal photoreceptor cells in rhodopsin P347L transgenic rabbits. Calpain-1 C2L结构域肽对红紫质P347L转基因家兔视网膜感光细胞的保护作用

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-12 DOI: 10.1016/j.exer.2026.110862

On Kosegawa, Yusaku Chukai, Minami Shimokawara, Nanami Furukawa, Tetsuro Yamashita, Taku Ozaki

Retinitis pigmentosa (RP) leads to visual impairment by causing the death of photoreceptor cells. Mitochondrial calpain-1, an intracellular enzyme dependent on Ca²⁺ signaling, induces cell death in RP by cleaving and releasing apoptosis-inducing factors from the mitochondria. Previously, we developed Tat-μCL, a mitochondrial calpain-1 inhibitor that protects the retina from degeneration in a rat model of RP. Herein, we investigated its effect on a rabbit model of RP, which is more human-like than the rat model. We used a transgenic (Tg) rabbit harboring a P347L rhodopsin mutation and applied saline or Tat-μCL to each eye of the Tg rabbit using eye drops. Before and after 8 and 16 weeks of saline or Tat-μCL instillation, we performed electroretinography (ERG) and optical coherence tomography (OCT). After measurement in week 16, each eye was collected and histologically analyzed using hematoxylin and eosin (HE) staining and immunostaining for glial fibrillary acidic protein, ionized calcium-binding adapter molecule 1, apoptosis-inducing factor, and Tat-μCL. Tat-μCL substantially inhibited retinal thinning as determined via OCT and tended to improve the amplitude of the a- and b-waves in ERG measurement compared to saline. HE staining showed that Tat-μCL preserved the number of nuclear layers in the outer nuclear layer of the retina. Mitochondrial calpain-1 inhibition using Tat-μCL as eye drops prevented retinal degeneration in Tg rabbits, similar to our previous results from the rat model. These results validate our earlier findings that Tat-μCL preserves photoreceptor cells and delays disease progression in RP. Our findings need further validation in clinical settings.

色素性视网膜炎（RP）通过引起感光细胞的死亡而导致视力障碍。线粒体calpain-1是一种依赖于Ca2+信号的细胞内酶，通过从线粒体中切割和释放凋亡诱导因子来诱导RP中的细胞死亡。在此之前，我们开发了Tat-μCL，一种线粒体calpain-1抑制剂，可以保护视网膜免受RP大鼠模型的退化。在此，我们研究了其对兔RP模型的影响，该模型比大鼠模型更像人。我们使用含有P347L视紫红质突变基因的转基因（Tg）家兔，用滴眼液将生理盐水或Tat μ cl分别滴在Tg家兔的每只眼睛上。在生理盐水或Tat μ cl滴注8和16周前后，我们分别进行视网膜电图（ERG）和光学相干断层扫描（OCT）。第16周测量后，采集每只眼，采用苏木精和伊红（HE）染色和免疫染色对胶质纤维酸性蛋白、离子钙结合转接器分子1、凋亡诱导因子、Tat-μCL进行组织学分析。通过OCT检测，Tat μ cl显著抑制视网膜变薄，与生理盐水相比，在ERG测量中有改善a波和b波振幅的趋势。HE染色显示Tat-μCL保留了视网膜外核层的核层数。用Tat μ cl作为滴眼液抑制线粒体calpain-1可防止Tg家兔视网膜变性，与我们之前在大鼠模型中的结果相似。这些结果证实了我们早期的发现，即Tat-μCL可以保存感光细胞并延缓RP的疾病进展。我们的发现需要在临床环境中进一步验证。

{"title":"Calpain-1 C2L domain peptide protects retinal photoreceptor cells in rhodopsin P347L transgenic rabbits.","authors":"On Kosegawa, Yusaku Chukai, Minami Shimokawara, Nanami Furukawa, Tetsuro Yamashita, Taku Ozaki","doi":"10.1016/j.exer.2026.110862","DOIUrl":"https://doi.org/10.1016/j.exer.2026.110862","url":null,"abstract":"<p><p>Retinitis pigmentosa (RP) leads to visual impairment by causing the death of photoreceptor cells. Mitochondrial calpain-1, an intracellular enzyme dependent on Ca<sup>2+</sup> signaling, induces cell death in RP by cleaving and releasing apoptosis-inducing factors from the mitochondria. Previously, we developed Tat-μCL, a mitochondrial calpain-1 inhibitor that protects the retina from degeneration in a rat model of RP. Herein, we investigated its effect on a rabbit model of RP, which is more human-like than the rat model. We used a transgenic (Tg) rabbit harboring a P347L rhodopsin mutation and applied saline or Tat-μCL to each eye of the Tg rabbit using eye drops. Before and after 8 and 16 weeks of saline or Tat-μCL instillation, we performed electroretinography (ERG) and optical coherence tomography (OCT). After measurement in week 16, each eye was collected and histologically analyzed using hematoxylin and eosin (HE) staining and immunostaining for glial fibrillary acidic protein, ionized calcium-binding adapter molecule 1, apoptosis-inducing factor, and Tat-μCL. Tat-μCL substantially inhibited retinal thinning as determined via OCT and tended to improve the amplitude of the a- and b-waves in ERG measurement compared to saline. HE staining showed that Tat-μCL preserved the number of nuclear layers in the outer nuclear layer of the retina. Mitochondrial calpain-1 inhibition using Tat-μCL as eye drops prevented retinal degeneration in Tg rabbits, similar to our previous results from the rat model. These results validate our earlier findings that Tat-μCL preserves photoreceptor cells and delays disease progression in RP. Our findings need further validation in clinical settings.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110862"},"PeriodicalIF":2.7,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Therapeutic effect of nitazoxanide on Acanthamoeba keratitis in an experimental model. nitazoxanide治疗棘阿米巴角膜炎的实验模型。

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-10 DOI: 10.1016/j.exer.2026.110858

Toqa Yasser Shakour, Ahmad Ali Othman, Iman Abdel Fattah Fahmy, Ahmed Yousef Amin Ali, Asmaa Mostafa Mohamed Eid, Eman Sayed Elwakil, Hager S Zoghroban

Acanthamoeba keratitis (AK) is a severe infection caused by opportunistic protozoa called Acanthamoeba species, especially in contact lens wearers and immunocompromised people. The aim of the study was to assess the therapeutic efficiency of two nitazoxanide (NTZ) formulations in treating experimentally induced AK. Seven groups of 31 male New Zealand white rabbits were formed: Group (A-s) was infected and administered NTZ in suspension form; Group (A-c): the control group of the previous; Group (B-s): infected and administered NTZ in liquid crystal forming system; Group (B-c): the control group of the previous; Group (C-s): infected and administered topical chlorhexidine 0.02%; Group (C-c): the control group of the previous and Group (D): a normal control group. The effects of treatment were assessed over 30 days through daily clinical evaluation, grading of AK, parasitological and histopathological examination of corneal tissues. The present work revealed that after inducing keratitis, signs of infection appeared by day 3, and all groups showed similar infection rates before treatment began. Corneal opacity improved significantly in NTZ liquid crystal form- treated group, especially by days 18 to 30, showing outcomes comparable or superior to the chlorhexidine-treated group and markedly better than the NTZ suspension- treated group. Histopathological analysis confirmed these findings, with the NTZ liquid crystal group exhibiting minimal inflammation and no detectable cysts, highlighting its potential as an effective alternative treatment for AK.

棘阿米巴角膜炎（AK）是一种由棘阿米巴原虫引起的严重感染，特别是在隐形眼镜佩戴者和免疫功能低下的人群中。目的是评价两种硝唑尼特（NTZ）制剂治疗实验性AK的疗效。将雄性新西兰大白兔31只分为7组：A-s组感染后给予NTZ悬浮液；组（A-c）：前一组的对照组；B-s组：感染并给药NTZ液晶形成系统；B-c组：前两组的对照组；C-s组：感染后外用0.02%氯己定；组（C-c）：前一组的对照组；组(D)：正常对照组。通过日常临床评价、AK评分、角膜组织寄生虫学和组织病理学检查，在30天内评估治疗效果。本研究发现，在诱导角膜炎后，在第3天出现感染迹象，并且所有组在治疗开始前的感染率相似。NTZ液晶形态处理组角膜混浊明显改善，特别是在第18 ~ 30天，其结果与氯己定处理组相当或优于，明显优于NTZ混悬液处理组。组织病理学分析证实了这些发现，NTZ液晶组表现出最小的炎症和未检测到的囊肿，突出了其作为AK有效替代治疗的潜力。

{"title":"Therapeutic effect of nitazoxanide on Acanthamoeba keratitis in an experimental model.","authors":"Toqa Yasser Shakour, Ahmad Ali Othman, Iman Abdel Fattah Fahmy, Ahmed Yousef Amin Ali, Asmaa Mostafa Mohamed Eid, Eman Sayed Elwakil, Hager S Zoghroban","doi":"10.1016/j.exer.2026.110858","DOIUrl":"https://doi.org/10.1016/j.exer.2026.110858","url":null,"abstract":"<p><p>Acanthamoeba keratitis (AK) is a severe infection caused by opportunistic protozoa called Acanthamoeba species, especially in contact lens wearers and immunocompromised people. The aim of the study was to assess the therapeutic efficiency of two nitazoxanide (NTZ) formulations in treating experimentally induced AK. Seven groups of 31 male New Zealand white rabbits were formed: Group (A-s) was infected and administered NTZ in suspension form; Group (A-c): the control group of the previous; Group (B-s): infected and administered NTZ in liquid crystal forming system; Group (B-c): the control group of the previous; Group (C-s): infected and administered topical chlorhexidine 0.02%; Group (C-c): the control group of the previous and Group (D): a normal control group. The effects of treatment were assessed over 30 days through daily clinical evaluation, grading of AK, parasitological and histopathological examination of corneal tissues. The present work revealed that after inducing keratitis, signs of infection appeared by day 3, and all groups showed similar infection rates before treatment began. Corneal opacity improved significantly in NTZ liquid crystal form- treated group, especially by days 18 to 30, showing outcomes comparable or superior to the chlorhexidine-treated group and markedly better than the NTZ suspension- treated group. Histopathological analysis confirmed these findings, with the NTZ liquid crystal group exhibiting minimal inflammation and no detectable cysts, highlighting its potential as an effective alternative treatment for AK.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110858"},"PeriodicalIF":2.7,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145959223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comment on “Precise biometric measurement of the mouse eye using optical coherence tomography based on optic-nerve-head imaging” 评论“基于视神经头成像的光学相干断层扫描对小鼠眼睛的精确生物测量”。

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-08 DOI: 10.1016/j.exer.2026.110856

Zhili Cui , Jun Kang

引用次数: 0

miR-29b-3p promotes the recovery of alkali-burned cornea by targeting Ddx3x miR-29b-3p通过靶向Ddx3x促进碱烧伤角膜的恢复

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-08 DOI: 10.1016/j.exer.2026.110849

Juan Gao , Jun Li , Jinghua Liu , Ruifang Han , Xi Chen , Liming Wang , Yunqing Ma , Xuan Li

Corneal alkali burns often cause vision impairment by triggering excessive inflammation and fibrosis, which compromise corneal transparency. Given miR-29b-3p′s anti-inflammatory and anti-fibrotic properties, this study evaluated its therapeutic potential in corneal alkali injury. A murine corneal alkali burn model was established, and differentially expressed proteins were analyzed using liquid chromatography-mass spectrometry (LC-MS) at 24 h and 1-week post-injury. The results showed corneas exhibited both continuous and phase-specific pathway alterations during different stages of alkali burn recovery. We overexpressed miR-29b-3p in primary mouse bone marrow mesenchymal stem cells and isolated miR-29b-3p-enriched exosomes for delivery. Treatment with miR-29b-3p significantly accelerated corneal epithelial repair, reduced edema, and improved histological outcomes compared to controls. Bioinformatic analysis identified Ddx3x, Vcl, Col1a1, and Col6a2 as key candidate targets of miR-29b-3p. Among these, Ddx3x exhibited significant downregulation upon miR-29b-3p treatment in both murine corneas and human corneal epithelial cells (HCE). A dual-luciferase assay confirmed direct binding of miR-29b-3p to the 3′UTR of Ddx3x, suppressing its expression. Gene set enrichment analysis (GSEA) revealed that Ddx3x upregulates biosynthetic and secretory pathways while suppressing myofibril assembly. These findings identify miR-29b-3p as a promising therapeutic agent for corneal alkali burns, with Ddx3x as a critical downstream target. This study provides novel mechanistic insights into corneal alkali burn and proposes potential target for clinical intervention.

角膜碱烧伤通常会引起过度的炎症和纤维化，从而损害角膜的透明度，从而导致视力损害。鉴于miR-29b-3p的抗炎和抗纤维化特性，本研究评估了其在角膜碱损伤中的治疗潜力。建立小鼠角膜碱烧伤模型，分别在伤后24 h和1周采用液相色谱-质谱法（LC-MS）分析差异表达蛋白。结果表明，在碱烧伤恢复的不同阶段，角膜表现出连续的和阶段性的通路改变。我们在原代小鼠骨髓间充质干细胞中过表达miR-29b-3p，并分离富集miR-29b-3p的外泌体进行递送。与对照组相比，miR-29b-3p治疗可显著加速角膜上皮修复，减少水肿，改善组织学结果。生物信息学分析发现，Ddx3x、Vcl、Col1a1和Col6a2是miR-29b-3p的关键候选靶点。其中，Ddx3x在小鼠角膜和人角膜上皮细胞（HCE）中对miR-29b-3p处理均表现出显著下调。双荧光素酶测定证实miR-29b-3p与Ddx3x的3'UTR直接结合，抑制其表达。基因集富集分析（GSEA）显示，Ddx3x上调生物合成和分泌途径，同时抑制肌原纤维组装。这些发现确定了miR-29b-3p是角膜碱烧伤的一种有前景的治疗剂，而Ddx3x是一个关键的下游靶点。本研究为角膜碱烧伤提供了新的机制见解，并提出了临床干预的潜在靶点。

{"title":"miR-29b-3p promotes the recovery of alkali-burned cornea by targeting Ddx3x","authors":"Juan Gao , Jun Li , Jinghua Liu , Ruifang Han , Xi Chen , Liming Wang , Yunqing Ma , Xuan Li","doi":"10.1016/j.exer.2026.110849","DOIUrl":"10.1016/j.exer.2026.110849","url":null,"abstract":"<div><div>Corneal alkali burns often cause vision impairment by triggering excessive inflammation and fibrosis, which compromise corneal transparency. Given miR-29b-3p′s anti-inflammatory and anti-fibrotic properties, this study evaluated its therapeutic potential in corneal alkali injury. A murine corneal alkali burn model was established, and differentially expressed proteins were analyzed using liquid chromatography-mass spectrometry (LC-MS) at 24 h and 1-week post-injury. The results showed corneas exhibited both continuous and phase-specific pathway alterations during different stages of alkali burn recovery. We overexpressed miR-29b-3p in primary mouse bone marrow mesenchymal stem cells and isolated miR-29b-3p-enriched exosomes for delivery. Treatment with miR-29b-3p significantly accelerated corneal epithelial repair, reduced edema, and improved histological outcomes compared to controls. Bioinformatic analysis identified Ddx3x, Vcl, Col1a1, and Col6a2 as key candidate targets of miR-29b-3p. Among these, Ddx3x exhibited significant downregulation upon miR-29b-3p treatment in both murine corneas and human corneal epithelial cells (HCE). A dual-luciferase assay confirmed direct binding of miR-29b-3p to the 3′UTR of Ddx3x, suppressing its expression. Gene set enrichment analysis (GSEA) revealed that Ddx3x upregulates biosynthetic and secretory pathways while suppressing myofibril assembly. These findings identify miR-29b-3p as a promising therapeutic agent for corneal alkali burns, with Ddx3x as a critical downstream target. This study provides novel mechanistic insights into corneal alkali burn and proposes potential target for clinical intervention.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110849"},"PeriodicalIF":2.7,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145922265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Glucose exposure suppresses brain aromatase and impairs retinal regeneration in zebrafish 葡萄糖暴露抑制斑马鱼脑芳香化酶和损害视网膜再生。

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-07 DOI: 10.1016/j.exer.2026.110853

Zulvikar Syambani Ulhaq , Kazufumi Takamune , Mitsuyo Kishida

Zebrafish possess a unique capacity for retinal regeneration mediated by Müller glia (MG), in which the estrogen-synthesizing enzyme aromatase B (AroB, encoded by cyp19a1b) plays an important regulatory role. In this study, we investigated the impact of chronic glucose exposure on MG-driven retinal regeneration following mechanical injury. We found that AroB was expressed across multiple retinal layers, including the ganglion cell layer (GCL), inner nuclear layer (INL), outer nuclear layer (ONL), and both plexiform layers. Within the INL AroB colocalized with glutamine synthetase (GS)⁺ MG in controls, but was significantly suppressed in retinas exposed to 3 % glucose, a reduction corroborated by Western blot analysis, qRT-PCR, and measurements of E₂ levels. Retinal injury induced an upregulation of AroB and GS expression and triggered robust MG proliferation in controls, as indicated by EdU incorporation. In contrast, glucose exposure reduced the number of EdU⁺ proliferating cells, and colocalization of AroB⁺/MG⁺ with EdU⁺ nuclei was absent in the injured glucose-treated group. BrdU labeling performed 3 h before sacrifice revealed ongoing proliferation that followed a similar pattern to EdU, except that BrdU⁺ cells in glucose-exposed injured retinas eventually reached levels comparable to injured controls, suggesting a delay in regenerative proliferation. TUNEL staining showed significantly higher numbers of apoptotic cells in injured glucose-exposed retinas compared with injured controls, while no differences were detected between uninjured groups. Together, these findings demonstrate that chronic glucose exposure suppresses AroB expression, impairs early MG activation, delays regenerative proliferation, and exacerbates cell death after retinal injury, highlighting a potential mechanism by which hyperglycemia compromises endogenous retinal repair and contributes to diabetic retinopathy (DR). Nonetheless, given humans’ limited regenerative capacity, these mechanisms may not directly translate but still reveal pathways that could aid retinal repair in mammals.

斑马鱼具有独特的视网膜再生能力，这种能力是由 ller胶质细胞（MG）介导的，其中由cyp19a1b编码的雌激素合成酶芳香化酶B （AroB）起着重要的调节作用。在这项研究中，我们研究了慢性葡萄糖暴露对机械损伤后mg驱动的视网膜再生的影响。我们发现AroB在视网膜多层表达，包括神经节细胞层（GCL）、内核层（INL）、外核层（ONL）和两个丛状层。在INL中，AroB在对照中与谷氨酰胺合成酶(GS)+ MG共定位，但在暴露于3%葡萄糖的视网膜中被显著抑制，Western blot分析、qRT-PCR和E2水平测量证实了这种减少。EdU掺入表明，在对照组中，视网膜损伤诱导AroB和GS表达上调，并引发强劲的MG增殖。相比之下，葡萄糖暴露减少了EdU+增殖细胞的数量，并且在损伤的葡萄糖处理组中没有AroB+/MG+与EdU+核的共定位。牺牲前3小时进行的BrdU标记显示，与EdU类似的模式持续增殖，除了葡萄糖暴露的损伤视网膜中的BrdU+细胞最终达到与损伤对照组相当的水平，表明再生增殖延迟。TUNEL染色显示，与损伤对照组相比，葡萄糖暴露损伤视网膜中凋亡细胞数量明显增加，而未损伤组之间无差异。总之，这些研究结果表明，慢性葡萄糖暴露抑制AroB表达，损害早期MG激活，延迟再生增殖，并加剧视网膜损伤后的细胞死亡，突出了高血糖损害内源性视网膜修复并导致糖尿病视网膜病变（DR）的潜在机制。尽管如此，鉴于人类有限的再生能力，这些机制可能不能直接翻译，但仍然揭示了有助于哺乳动物视网膜修复的途径。

{"title":"Glucose exposure suppresses brain aromatase and impairs retinal regeneration in zebrafish","authors":"Zulvikar Syambani Ulhaq , Kazufumi Takamune , Mitsuyo Kishida","doi":"10.1016/j.exer.2026.110853","DOIUrl":"10.1016/j.exer.2026.110853","url":null,"abstract":"<div><div>Zebrafish possess a unique capacity for retinal regeneration mediated by Müller glia (MG), in which the estrogen-synthesizing enzyme aromatase B (AroB, encoded by <em>cyp19a1b</em>) plays an important regulatory role. In this study, we investigated the impact of chronic glucose exposure on MG-driven retinal regeneration following mechanical injury. We found that AroB was expressed across multiple retinal layers, including the ganglion cell layer (GCL), inner nuclear layer (INL), outer nuclear layer (ONL), and both plexiform layers. Within the INL AroB colocalized with glutamine synthetase (GS)<sup>+</sup> MG in controls, but was significantly suppressed in retinas exposed to 3 % glucose, a reduction corroborated by Western blot analysis, qRT-PCR, and measurements of E<sub>2</sub> levels. Retinal injury induced an upregulation of AroB and GS expression and triggered robust MG proliferation in controls, as indicated by EdU incorporation. In contrast, glucose exposure reduced the number of EdU<sup>+</sup> proliferating cells, and colocalization of AroB<sup>+</sup>/MG<sup>+</sup> with EdU<sup>+</sup> nuclei was absent in the injured glucose-treated group. BrdU labeling performed 3 h before sacrifice revealed ongoing proliferation that followed a similar pattern to EdU, except that BrdU<sup>+</sup> cells in glucose-exposed injured retinas eventually reached levels comparable to injured controls, suggesting a delay in regenerative proliferation. TUNEL staining showed significantly higher numbers of apoptotic cells in injured glucose-exposed retinas compared with injured controls, while no differences were detected between uninjured groups. Together, these findings demonstrate that chronic glucose exposure suppresses AroB expression, impairs early MG activation, delays regenerative proliferation, and exacerbates cell death after retinal injury, highlighting a potential mechanism by which hyperglycemia compromises endogenous retinal repair and contributes to diabetic retinopathy (DR). Nonetheless, given humans’ limited regenerative capacity, these mechanisms may not directly translate but still reveal pathways that could aid retinal repair in mammals.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110853"},"PeriodicalIF":2.7,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145942983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Investigation of the biomechanical changes at the iris-lens interface after vitrectomy with silicone oil tamponade: Insights from ultrasound biomicroscopy 硅油填塞玻璃体切除术后虹膜-晶状体界面生物力学变化的超声生物显微镜观察

IF 2.7 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research

Pub Date : 2026-01-07 DOI: 10.1016/j.exer.2026.110855

Jiajun Chen, Ling Wang, Long Tao, Shasha Xue, Yunxiao Wang, Fenglei Wang

This prospective cohort study investigated anterior segment biomechanical alterations and lens stability using ultrasound biomicroscopy (UBM) in 60 eyes (58 patients) undergoing pars plana vitrectomy (PPV) with silicone oil (SO) tamponade for rhegmatogenous (18 eyes) or diabetic tractional retinal detachment (42 eyes). UBM parameters, including central corneal thickness (CCT), anterior chamber depth (ACD), lens vault (LV), angle-opening distance (AOD500), trabecular-iris angle (TIA), iris-lens angle (ILA), and iris-lens contact distance (ILCD), were assessed preoperatively and 3 months postoperatively. Significant postoperative reductions were observed in CCT (−0.026 mm, P = 0.005), superior ILCD (0.921→0.730 mm, P = 0.006), inferior ILCD (0.914→0.702 mm, P = 0.002), and mean ILCD (0.947→0.745 mm, P = 0.001). The inferior ILA increased (20.31°→23.39°, P = 0.032), while the temporal ILA decreased (20.70°→18.29°, P = 0.047). Subgroup analysis comparing normotensive and hypertensive eyes revealed significant differences in nasal ΔILA (P = 0.008) and temporal ΔILCD (P = 0.014). Multiple regression identified a negative correlation between intraocular pressure (IOP) and nasal ΔILA (β = −0.353, P = 0.002). The findings demonstrate that PPV with SO tamponade induces significant biomechanical alterations at the iris-lens interface, compromising lens stability, and provide valuable anatomical insights for optimizing cataract surgery in SO-filled eyes.

本前瞻性队列研究采用超声生物显微镜（UBM）观察60眼（58例）玻璃体切割术（PPV）加硅油（SO）压塞治疗孔源性（18眼）或糖尿病牵引性视网膜脱离（42眼）的前段生物力学改变和晶状体稳定性。术前和术后3个月评估UBM参数，包括角膜中央厚度（CCT）、前房深度（ACD）、晶状体穹窿（LV）、角开口距离（AOD500）、小梁-虹膜角（TIA）、虹膜-晶状体角（ILA）、虹膜-晶状体接触距离（ILCD）。术后CCT （- 0.026 mm, P = 0.005）、上ILCD（0.921→0.730 mm, P = 0.006）、下ILCD（0.914→0.702 mm, P = 0.002）、平均ILCD（0.947→0.745 mm, P = 0.001）均显著降低。下侧ILA增大（20.31°→23.39°，P = 0.032），颞侧ILA减小（20.70°→18.29°，P = 0.047）。亚组分析结果显示，正常眼和高血压眼的鼻部ΔILA （P = 0.008）和颞部ΔILCD （P = 0.014）差异有统计学意义。多元回归发现眼压（IOP）与鼻腔ΔILA呈负相关（β = - 0.353, P = 0.002）。研究结果表明，有SO填塞的PPV在虹膜-晶状体界面引起了显著的生物力学改变，影响了晶状体的稳定性，并为优化SO填充眼的白内障手术提供了有价值的解剖学见解。

{"title":"Investigation of the biomechanical changes at the iris-lens interface after vitrectomy with silicone oil tamponade: Insights from ultrasound biomicroscopy","authors":"Jiajun Chen, Ling Wang, Long Tao, Shasha Xue, Yunxiao Wang, Fenglei Wang","doi":"10.1016/j.exer.2026.110855","DOIUrl":"10.1016/j.exer.2026.110855","url":null,"abstract":"<div><div>This prospective cohort study investigated anterior segment biomechanical alterations and lens stability using ultrasound biomicroscopy (UBM) in 60 eyes (58 patients) undergoing pars plana vitrectomy (PPV) with silicone oil (SO) tamponade for rhegmatogenous (18 eyes) or diabetic tractional retinal detachment (42 eyes). UBM parameters, including central corneal thickness (CCT), anterior chamber depth (ACD), lens vault (LV), angle-opening distance (AOD500), trabecular-iris angle (TIA), iris-lens angle (ILA), and iris-lens contact distance (ILCD), were assessed preoperatively and 3 months postoperatively. Significant postoperative reductions were observed in CCT (−0.026 mm, P = 0.005), superior ILCD (0.921→0.730 mm, P = 0.006), inferior ILCD (0.914→0.702 mm, P = 0.002), and mean ILCD (0.947→0.745 mm, P = 0.001). The inferior ILA increased (20.31°→23.39°, P = 0.032), while the temporal ILA decreased (20.70°→18.29°, P = 0.047). Subgroup analysis comparing normotensive and hypertensive eyes revealed significant differences in nasal ΔILA (P = 0.008) and temporal ΔILCD (P = 0.014). Multiple regression identified a negative correlation between intraocular pressure (IOP) and nasal ΔILA (β = −0.353, P = 0.002). The findings demonstrate that PPV with SO tamponade induces significant biomechanical alterations at the iris-lens interface, compromising lens stability, and provide valuable anatomical insights for optimizing cataract surgery in SO-filled eyes.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110855"},"PeriodicalIF":2.7,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145922266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0