补肾活血中药对大鼠慢性高眼压模型视神经病理改变的影响

目的 观察补肾活血中药对大鼠慢性高眼压(elevated intraocular pressure,EIOP)模型视神经损伤的干预作用,探讨其作用机理.方法 30只(30眼)SD大鼠采用烙闭上巩膜静脉法建立大鼠慢性EIOP模型,随机分为三组:对照组、模型组、给药组,每组各10只,观察补肾活血中药对EIOP大鼠眼压(intraocular pressure,IOP)、视神经病理形态学变化以及超微结构的影响.结果 本实验采用的烙闭上巩膜静脉法使大鼠IOP明显升高(均为P＜0.01),在造模后8周(实验结束)lOP仍为造模前的2～3倍;视神经病理切片半定量分析表明:视神经纤维髓鞘总面积、平均光密度值及积分光密度值分别为:模型组(98 048.810±8139.059) μm2、(517.840±118.862)、(18 031.320±1895.210),对照组各指标分别为(144 975.320±10 341.487) μm2、(768.700±167.331)、(29 283.350±2331.446),两组间比较差异均有统计学意义(均为P＜0.05);给药组各指标分别为(109 420.500±55 263.250) μm2、(710.080±150.956)、(24 225.730±5455.363),与模型组各指标比较,差异均有统计学意义(均为P＜0.05);模型组大鼠视神经超微结构损害明显,给药组损害有所改善.结论 补肾活血中药有助于EIOP大鼠视神经损伤的修复.     

慢性高眼压对兔眼视神经的影响

本实验对２２只（４４只眼）健康成年青紫蓝兔的视神经乳头，在持续不同时间的高眼压状态下，分别进行了光镜和电镜的观察。     

葡萄糖调节蛋白在急性高眼压大鼠视网膜中的表达及其意义

背景 青光眼导致的视网膜神经节细胞(RGCs)进行性死亡是导致患者视功能损害的主要病理基础,研究表明内质网应激(ERS)参与此过程,葡萄糖调节蛋白78( GRP78)是内质网中的特异性标志物,检测GRP78在高眼压诱导视网膜中的表达对青光眼患者视神经功能保护机制的研究具有重要意义. 目的 检测GRP78在大鼠急性高眼压后不同时期视网膜中的表达情况,探讨ERS在急性青光眼损伤中的作用.方法 56只Wistar大鼠采用随机数字表法分为正常对照组、前房穿刺组、急性高眼压12h组及急性高眼压1、3、7、14 d组,每组8只眼.急性高眼压模型的制作采用前房穿刺灌注生理盐水法,眼压提高至66 mmHg.分别于造模后12h及1、3、7、14 d用过量麻醉法处死大鼠.苏木精-伊红染色法观察各组大鼠视网膜的病理形态学改变;免疫组织化学法检测视网膜中的GRP78蛋白表达的变化;实时定量逆转录聚合酶链反应(RTPCR)法检测视网膜中GRP78 mRNA的表达变化. 结果 正常对照组大鼠视网膜各层细胞排列整齐,急性高眼压后12h视网膜水肿增厚、细胞核肿胀,1d时视网膜形态学异常改变达到高峰,3d后水肿减轻,视网膜变薄.免疫组织化学染色显示正常对照组、前房穿刺组大鼠RGCs层和内核层GRP78蛋白呈弱阳性表达,A值分别为0.195±0.006、0.196±0.005,急性高眼压12h组大鼠GRP78在视网膜的表达明显增强,A值为0.293±0.011,造模后1d时GRP78表达强度达到高峰,A值为0.499±0.039,造模后3d时GRP78表达明显降低,A值为0.268±0.017,与正常对照组大鼠比较差异均有统计学意义(t=0.098、0.304、0.073,P＜0.05),但造模后7d和14 d时GRP78在大鼠视网膜RGCs层和内核层中的表达量接近正常,与正常对照组比较差异均无统计学意义( t=0.002、0.001,P＞0.05).实时定量RT-PCR检测表明,GRP78 mRNA在正常对照组大鼠视网膜的相对表达量( 2-△△CT)为1.011±0.013,眼压升高12 h快速上调,为1.536±0.145,1 d时达高峰,为2.141±0.171,3d时迅速降低,为1.420±0.212,与正常对照组比较差异均有统计学意义(t=0.525、1.130、0.409,P＜0.05),而造模后7d及14 d GRP78 mRNA在大鼠视网膜的表达量明显下降,与正常对照组比较差异均无统计学意义(t=0.020.0.004,P＞0.05).结论 GRP78参与大鼠急性高眼压后视网膜损伤的发生机制,提示通过对ERS过程进行干预可能达到保护急性高眼压眼视神经功能的目的.     

青光眼模型视神经损伤的评估方法

对青光眼动物模型视神经损伤的评估有利于青光眼发病机制和治疗方法的研究.目前主要从视网膜神经节细胞(retinal ganglion cell,RGC)计数、视网膜内层厚度测定和球后视神经轴突计数三方面进行评估.几种评估方法各有优缺点.RGC的凋亡直接反映视神经损伤的程度,视网膜全铺片染色计数RGC方法操作较简单,但视网膜铺片各层细胞易于重叠;逆行荧光染料标记需进行颅内手术且染料可能泄露到邻近小胶质细胞,导致不准确的计数;视网膜厚度测量不能直接反映视神经损伤的程度;视神经轴突计数难度相对较高;体视学方法可直接计数RGC,但需要熟悉相关体视学公式及方法,目前在该领域的报道较少.     

慢性高眼压兔模型视网膜中生长相关蛋白-43表达的变化

目的:研究持续高眼压状态下视网膜中生长相关蛋白-4(GAP-43)表达的变化。方法:兔眼前房注射复方卡波姆溶液制成慢性高眼压模型(n=21),用免疫组织化学方法观察在高眼压不同时间段视网膜中GAP-43的表达变化。结果:正常兔眼视网膜内丛状层中存在GAP-43的表达。持续性高眼压7d后内丛状层中的GAP-43免疫反应产物密度增加,且在节细胞和神经纤维层也出现阳性产物,与对照组比较有显著差异(P<0.05)。高眼压14d时阳性反应产物与7d时相比有所下降,但仍高于正常对照组(P<0.05);21d时基本恢复至正常对照组水平(P>0.05)。结论:慢性高眼压时视神经、视网膜结构受损,导致视网膜中GAP-43短暂升高。     

慢性高眼压模型鼠视网膜神经节细胞及视神经中9位丝氨酸磷酸化糖原合酶激酶3β的表达变化

目的 观察慢性高眼压模型鼠视网膜神经节细胞(retina ganglion cells,RGCs)和视神经中9位丝氨酸磷酸化糖原合酶激酶3β[p-GSK3β(ser9)]的表达变化,探讨GSK3β是否在慢性高眼压RGCs及视神经退行性病变中发挥作用.方法 取健康SD大鼠30只,随机分为3组:模型对照组、慢性高眼压模型2周组、慢性高眼压模型4周组,每组10只.取大鼠右眼,采用巩膜上静脉结扎并烧灼法建立大鼠慢性高眼压模型.分别于造模后2周和4周取5只大鼠眼球行冰冻切片,尼氏染色观察RGCs数目,免疫荧光染色观察RGCs和视神经中p-GSK3β(ser9)的变化;各组取另外5只大鼠眼视网膜,Western blot检测p-GSK3β(ser9)及总-GSK3β的表达.结果 造模前3组大鼠右眼眼压差异无统计学意义(P=0.89);造模后3组间眼压差异有统计学意义(P＜0.01),慢性高眼压模型2周组和4周组眼压与模型对照组比较明显升高,分别升高了59.13％和26.93％,差异均有统计学意义(均为P＜O.01).视网膜尼氏染色RGCs计数发现模型对照组RGCs数为(149±12)个,慢性高眼压模型2周组和4周组RGCs数较模型对照组明显减少,分别为(120±10)个和(86±7)个,差异均有统计学意义(均为P＜0.05);且4周组比2周组进一步减少(P＜0.01).慢性高眼压模型2周组和4周组视网膜中p-GSK3β(ser9)阳性着色,同模型对照组相比,其RGCs层及视神经中p-GSK3β(ser9)染色荧光减弱;4周组较模型对照组减弱更明显.与模型对照组相比,慢性高眼压模型2周组和4周组视网膜中总-GSK3β的表达差异无统计学意义(F=0.24,P=0.79);而3组间p-GSK3β(ser9)表达差异有统计学意义(P＜0.01),与模型对照组相比,慢性高眼压模型2周组和4周组视网膜中p-GSK3β(ser9)分别减少了19.89％和36.46％(均为P ＜0.05).慢性高眼压模型4周组比2周组视网膜中p-GSK3β(ser9)表达持续减少,差异具有统计学意义(P＜0.05).结论 慢性高眼压模型鼠RGCs数目减少,RGCs和视神经中p-GSK3β(ser9)表达减少,推测p-GSK3β(ser9)表达变化可能参与了慢性高眼压模型鼠RGCs及视神经退行性病变.     

补精益视片对大鼠慢性高眼压模型视网膜p-Akt表达的影响

目的　观察补精益视片对大鼠慢性高眼压（ｅｌｅｖａｔｅｄｉｎｔｒａｏｃｕｌａｒｐｒｅｓｓｕｒｅ,ＥＩＯＰ）模型ｐ-Ａｋｔ表达的干预作用,探讨其作用机理。方法　将３０只ＳＤ大鼠随机分为３组:对照组、模型组、给药组,模型组和给药组采用烙闭上巩膜静脉法建立ＳＤ大鼠慢性ＥＩＯＰ模型,给药组每天予１．８ｇ·ｋｇ－１体质量补精益视片混悬液灌胃,对照组、模型组每天予３ｍＬ生理盐水灌胃,连续给药８周,并于８周末处死大鼠,观察各组大鼠眼压、视网膜ｐ-Ａｋｔ表达的情况。结果　模型组、给药组大鼠造模后即刻直至造模后８周与造模前眼压相比均升高,差异均有统计学意义（均为Ｐ＜０．０１）;造模后８周眼压与造模后即刻相比,给药组有降低趋势,差异有统计学意义（Ｐ＜０．０１）,模型组无降低趋势,差异无统计学意义（Ｐ＞０．０５）。造模后８周视网膜ｐ-Ａｋｔ表达免疫组织化学分析示:给药组总面积、平均光密度和积分光密度分别为（７４６３１．８１±１２８４１．３０）μｍ２,９３９．２６±１７５．１７和３７８１４．９６±５８２２．７１,与模型组的（３７９４７．２６±８０５０．５１）μｍ２、４８１．４５±１６１．０２和１８９０７．６４±４３６７．２９相比,差异均有显著统计学意义（均为Ｐ＜０．０１）;给药组平均黑度为１３８．５５±８．５８,虽高于模型组的１３６．５２±３．８１,但差异无统计学意义（Ｐ＞０．０５）。结论　补精益视片通过降低眼压、上调视网膜ＰＩ３Ｋ／Ａｋｔ信号转导通路中ｐ-Ａｋｔ的表达而保护慢性ＥＩＯＰ模型ＳＤ大鼠的视功能。     

大鼠慢性高眼压青光眼模型的构建及鉴定

目的:手术建立慢性高眼压青光眼大鼠模型对研究青光眼发病机制、治疗和视神经保护这三方面的研究尤为必要。方法:烧灼3条表浅巩膜静脉,并术中联合应用结膜瓣下浸有0.2g/L的丝裂霉素的凝胶海绵,阻断大鼠的眼部房水外流,建立大鼠慢性高眼压模型,手术后2h;1,3,7,14,28,56d处死5只大鼠,空白对照组亦处死5只大鼠;摘除眼球光镜下进行视网膜形态的观察及视网膜厚度测量,研究眼压、视网膜神经节细胞(retinal ganglion cells,RGC)和视神经损伤的特性。结果:大鼠手术眼与假手术眼、空白对照眼的术后各时间点的眼压比较差异有显著性(P<0.01)。结论:建立大鼠慢性高眼压模型操作简单,重复性好,成模率高,高眼压可稳定维持长时间,慢性高眼压将导致整个视网膜的变薄和萎缩。     

高眼压性青光眼压动物模型

青光眼是一类非常复杂的眼病,高眼压是青光眼发生,发展的重要因素,本文就高眼压性青光眼模型,尤其是各种实验性青光眼的特点,诱导方法及结果进行综述,并介绍根据不同的研究目的,如何选用合适的模型。     

Histological observation of RGCs and optic nerve injury in acute ocular hypertension rats

AIM: To explore the injury of retinal ganglion cells (RGCs) and optic nerves in acute ocular hypertension (OHT) rats. METHODS: We retrogradely labeled RGCs and optic nerves of Sprague-Dawley rats by injecting 20g/L fluorogold (FG) into bilateral superior colliculi. Twenty-four hours after the injection, the right eyes were performed physiological saline anterior chamber perfusion with intraocular pressure maintained at 100mmHg for 60 minutes, while the contralateral eyes were performed sham procedure as control group without elevation of the saline bottle. Retinal hematoxylin and eosin (HE) sections, retinal whole mounts and frozen sections were made 14 days later to observe the morphology and survival of RGCs. Frozen sections and transmission electron microscopy were utilized to investigate the histological manifestations of optic nerves at the same time. RESULTS: A larger number of RGCs presented in control group. It had an average density of 1995±125/mm2 and distributed uniformly, while RGCs in OHT eyes reduced significantly to 1505±43/mm2 compared with control group (P<0.05). The optic nerves in control group showed stronger and more uniform fluorescence on the frozen sections, and the auxiliary fibers as well as myelin sheaths were in even and intact organization by transmission electron microscopy. However, exiguous fluorescence signals, vesicular dissociation and disintegration of myelin sheaths were found in OHT group. CONCLUSION: The present study suggested that fluorogold retrograde tracing is a feasible, convenient method for quantitative and qualitative study of neuronal populations and axonal injury in acute ocular hypertension rats.     

The assessment of structural changes on optic nerve head and macula in primary open angle glaucoma and ocular hypertension

AIM: To assess morphological changes in macula, retinal nerve fiber layer (RNFL) and optic nevre head (ONH) of cases with primary open angle glaucoma (POAG) and ocular hypertension (OH) with spectral domain optic coherence tomography (OCT). METHODS: This study included 109 eyes from 62 POAG patients, 50 eyes from 30 OH patients, and 101 eyes from 53 healthy volunteers. Data gained by OCT were compared with perimetry indexes. ONH, RNFL and macula analysis were performed for all subjects. Rim area, disc area, average cup/disc (C/D) ratio, vertical C/D ratio, cup volume data were recorded during ONH analysis. Average RNFL thickness and the thickness of four quadrants (superior, inferior, nasal and temporal) was established in microns. In total, nine macular quadrants involving the foveal region mentioned in the Early Treatment Diabetic Treatment Study (ETDRS) template were measured, and average macular thickness and macular volume data were recorded during macula analysis. Differences between groups were evaluated with the one-way ANOVA test. Tukey’s multiple comparison test was performed to detect difference between groups. Receiver-operating characteristic (ROC) analysis was done for early stage POAG patients to establish sensitivity and specificity of chosen parameters in early stage POAG. Area under the receiver operating characteristic (AUROC) values were calculated to compare ROC areas. RESULTS: Statistically significant differences were found in all ONH parameters, except optic disc area. Neuroretinal rim area was identified as the parameter with the highest difference between groups (F=21.72, P<0.05). The highest correlation between ONH parameters and perimetry was observed at neuroretinal rim region (r=0.487). Inferior RNFL thickness was established as the parameter with the highest difference between groups among RNFL parameters. In the mean of all glaucoma patients, the highest correlation between data handled with OCT and mean deviation was observed in RNFL thickness. Average macular thickness was detected as the parameter with the highest difference between groups among macular parameters. The highest correlation between macula parameters and perimetry indexes was observed between average macular thickness and perimetry indexes (r=0.514). CONCLUSION: Although the assessment of ONH and the analysis of macular thickness are important in diagnosis and treatment, RNFL assessment is the most valuable parameter.     

Functional evaluation of retina and optic nerve in the rat model of chronic ocular hypertension

PURPOSE: To functionally characterize the rat retina and optic nerve after chronic elevation of the intraocular pressure (IOP) using electroretinography (ERG) and computerized pupillometry. METHODS: Chronic elevation of the IOP was induced in Brown Norway rats by combined injection of indocyanine green dye (ICG) into the anterior chamber and diode laser treatment, followed by ERG and pupil light reflex (PLR) monitoring. RESULTS: Laser treatment induced significant elevation of the IOP in operated eyes for 6 weeks, with maximal values observed 14 days postoperatively (ctrl=18.4+/-2.4 and operated=35+/-8.4 mmHg; mean+/-sd). Preoperative values for the PLR(ratio) were 68.5+/-4% (mean+/-sem; %). Three days postoperatively the PLR(ratio) decreased to 60.3+/-10.3%, but was not significantly different compared to preoperative values (p > 0.05 Kruskal-Wallis non-parametric test with Dunn's post-test). However, 7, 14 and 21 days postoperatively the PLR function dramatically decreased to 14.6+8.6, 11.5+/-6.7 and 12.6+/-4%, respectively, and was significantly smaller compared to preoperative values (p < 0.01). At day 28 the PLR significantly recovered and was not significantly different compared to preoperative values (PLR(ratio)=38.5+/-8.6, p > 0.05). However, 35 days after surgery the PLR started to decrease once again in the operated eyes (PLR(ratio)=17.2+/-7.4%) and was significantly smaller again compared to preoperative values (p < 0.05) The PLR values continued to decrease until the end of experiment (60 days postoperatively). ERG analysis of operated eyes revealed significantly decreased amplitudes of a- and b-waves 10d postoperatively, while oscillatory potentials (OPs) and flicker ERG (flERG) amplitudes were not detectable. However, 28 days postoperatively OPs significantly, but temporarily recovered, while a-wave, b-wave and flERG amplitudes did not significantly change compared to values observed 10d postoperatively. The ERG analysis of the operated eyes revealed significantly reduced amplitudes 60 days postoperatively. Histological analysis revealed degeneration of all retina layers and optic nerve axons. CONCLUSIONS: Chronic ocular hypertension in rats produces dramatic damage to all retinal layers and optic nerves observed by morphological and functional methods which significantly correlate with the IOP elevation. Outer retina of glaucomatous rats seems to be more susceptible to the damage due to chronic elevation of the IOP. Chronic hypertensive rat eyes have capacity to temporarily recover function of the inner retina and optic nerve.     

睫状神经营养因子和生长相关蛋白-43在兔眶内慢性视神经损伤中的表达

目的建立眶内视神经慢性受压损伤动物模型,并观察睫状神经营养因子（CNTF）和生长相关蛋白-43（GAP-43）在视神经中的表达。设计实验研究。研究对象新西兰大白兔36只。方法将动物分为6组,即A组（无压迫组）：只放置球囊而不充盈造影剂;B组（2w）：逐量注入造影剂压迫2周;C组（2w＋2w）：压迫2周后解除压迫2周;D组（4w）：注入造影剂压迫4周;E组（4w＋4w）：压迫4周解除压迫4周;F组（8W）：压迫8周。用眼眶内植入气囊并定时注入造影剂的方法,模拟眼眶肿瘤缓慢生长对眶内视神经慢性压迫,建立视神经慢性损伤动物模型;用RT—PCR方法检测在眶内视神经慢性损伤后不同阶段（造模后2、4、8周）CNTF和GAP-43的基因表达。主要指标CNTF和GAP．43的表达。结果眼底像和组织病理检查显示,随着压迫时间的延长,眼底、视网膜和视神经都出现病理改变并逐渐加重。空白及无压迫组低表达CNTF和GAP－43,压迫2周后即可见表达上调（P〈0．01）,随着压迫时间延长,两种基因均见表达逐渐增高（P〈0．01）。结论成功建立兔眶内视神经慢性损伤动物模型,并观察到随着压迫时间的延长,CNTF和GAP-43在视神经中的表达量逐渐增多,提示神经细胞被外来损伤诱导,开始进行自身修复。（眼科,2010．19：135—138）     

标准化大鼠外伤性视神经损伤动物模型建立

目的建立标准化外伤性视神经损伤动物模型。方法应用液压冲击颅脑损伤仪(FPI)分别以(6.9±0.6)atm和(2.4±0.2)atm的冲击力打击Wister大鼠右、左眼眶内贴近眼球部的视神经,建立两组程度不同的视神经损伤模型。通过闪光视觉诱发电位(F-VEP)、眼眶磁共振成像(MRI)、视网膜病理、视神经电镜等方法对正常及损伤后1、3d,1、2、4、6、8周大鼠的双眼进行检测。结果(1)损伤后大鼠F-VEP与伤前相比,潜伏期延长、振幅降低,此变化具有统计学意义(P<0.05)。损伤程度越重,伤后主波潜伏期延迟及振幅降低越明显,波形变化趋于稳定所需时间也越长。(2)伤后1 d眼眶MRI显示视神经受损部位信号增高、眶内结构紊乱;伤后8周视神经受损部位的高信号仍较明显、损伤部位靠近眼球侧视神经信号不均匀。轻、重两组差别不明显。(3)光镜下伤后1 d视网膜神经节细胞层(GCL)出血,伤后4周视网膜各层细胞稀疏、排列欠整齐,GCL散在核染色质浓集、边聚的节细胞,伤后8周视网膜各层细胞明显减少,GCL内大量空化节细胞。(4)电镜下损伤后4周视神经轴索萎缩变性,髓鞘肿胀、板层松解分离,伤后8周在血管和星形胶质细胞突起的附近有新生轴突,呈簇分布、生长良好。重伤组新生轴突枝芽少于轻伤组。结论应用FPI可以成功建立标准化大鼠外伤性视神经损伤动物模型。     

Evaluation of the nerve fiber layer and peripapillary atrophy in ocular hypertension

A study has been performed with the Canon retinographic equipment on 549 eyes belonging to 3 different groups: normal population, ocular hypertension and glaucoma. The study included the evaluation of the optic disk with special attention to the presence of choroidal peripapillary atrophy, and the distribution and defects in the RNFL.A highly significant association was observed between the presence of peripapillary atrophy and the presence of defects in the RNFL, as well as between the intensity of choroidal atrophy and defects in the RNFL.This association was statistically significant in the population of ocular hypertensives (P=0,0360) but not in the population of eyes considered normal.     

恒河猴慢性高眼压模型视乳头和视神经纤维损伤模式

目的 观察恒河猴慢性高眼压模型与开角型青光眼患者的视乳头和视神经纤维损伤模式是否一致。方法 实验研究。采用眼科多波长激光仪光凝恒河猴（12眼）的小梁网以破坏小梁网功能使眼压升高,建立恒河猴慢性高眼压模型。术前和术后每周行眼压、眼底照相、视乳头参数和视神经纤维层厚度检测。结果 建模的12眼术前眼压为（16.08±2.02）mmHg,中央角膜厚度为（489.17±17.82）μm,眼轴为（20.32±0.84）mm。12只用于诱导建模的恒河猴眼,经3～4次激光光凝,11眼被成功诱导。27周平均眼压为（30.32±14.59）mmHg,眼压波动幅度为（8.19±7.45）mmHg。光学相关断层扫描成像显示整个盘沿面积从（1.67±0.44）mm2减小到（0.43±0.34）mm2。平均视神经纤维从（97.92±6.79）μm减少到（64.46±17.44）μm。结论 恒河猴慢性高眼压性模型模拟了人类高眼压/开角型青光眼发病机制和过程,在视杯对高眼压的反应、视杯可逆性缩小、视神经纤维损伤现象等方面一致,是开展高眼压性视乳头和视神经纤维层损伤研究理想的动物模型。     

姜黄素对慢性高眼压大鼠视网膜神经节细胞凋亡的影响及机制

目的：探讨姜黄素对慢性高眼压大鼠视网膜神经节细胞(RGCs)凋亡的影响及机制。

方法：将21只SD大鼠随机分为3组,每组7只,高眼压模型组和姜黄素治疗组大鼠通过烧灼巩膜上静脉法建立慢性高眼压模型,假手术组大鼠仅剪开球结膜,不烧灼巩膜上静脉; 姜黄素治疗组给予4mL/kg姜黄素灌胃,假手术组和高眼压模型组给予4mL/kg纯水灌胃,连续3wk。造模后3wk,采用HE染色观察各组大鼠视网膜组织形态病理变化、RGCs数量及神经节细胞层(GCL)厚度; 采用TUNEL染色观察各组大鼠RGCs和视网膜细胞凋亡情况; 采用实时荧光定量PCR、免疫组织化学染色和Western blot法检测各组大鼠视网膜谷氨酰半胱氨酸连接酶调节亚基(GCLM)与血红素加氧酶-1(HO-1)的表达水平。

结果：与假手术组相比,高眼压模型组和姜黄素治疗组大鼠视网膜组织形态紊乱,RGCs数量减少,GCL变薄,RGCs和视网膜细胞凋亡率均升高,GCLM和HO-1表达量均升高; 与高眼压模型组相比,姜黄素治疗组大鼠视网膜组织形态基本正常,RGCs数量增多,GCL增厚,RGCs和视网膜细胞凋亡率均降低,GCLM和HO-1表达量均升高。

结论：姜黄素在慢性高眼压大鼠模型中可通过上调抗氧化基因GCLM与HO-1的表达抑制RGCs凋亡。