AG对大鼠慢性高眼压视网膜Caspase-9表达的影响

目的:研究慢性高眼压过程中大鼠视网膜Caspase-9表达的变化及应用AG对其表达的影响,探讨AG可能存在的对慢性高眼压视网膜的保护作用。方法:应用免疫组化、RT-PCR和Western blot的方法观察应用AG及未应用AG的慢性高眼压大鼠视网膜在慢性高眼压后不同时间点的形态学变化及Caspase-9表达的变化。结果:与正常对照组相比,随着高眼压时间的延长视网膜逐渐出现可察觉的形态学变化,于高眼压的第21d视网膜变薄,节细胞数量减少;在此过程中,Caspase-9表达增多,与形态学变化相一致。而应用AG者其形态学变化和Caspase-9表达变化较小。结论:凋亡相关基因Caspase-9在慢性高眼压视网膜损伤过程中发挥了作用,AG通过下调其表达对视网膜起保护作用。     

氨基胍对大鼠慢性高眼压视网膜NF-κB表达的影响

目的:研究慢性高眼压过程中大鼠视网膜核转录因子(NF-κB)表达的变化及应用氨基胍(amino guanidine,AG)对其表达的影响,探讨AG对慢性高眼压视网膜的保护作用。方法:应用免疫组化和Western blotting的方法观察应用及未应用AG的慢性高眼压大鼠视网膜在不同时点的形态学变化及NF-κB表达的变化。结果:随着高眼压时间的延长,视网膜逐渐变薄,节细胞数量减少;在此过程中,NF-κB表达增多。慢性高眼压大鼠的视网膜应用AG者与未应用AG者相比,其形态学变化较小,而NF-κB表达则明显增多。结论:NF-κB是慢性高眼压视网膜损伤过程中的保护性因素,AG通过上调其表达发挥对视网膜的保护作用。     

大鼠慢性高眼压下视网膜损伤中HIF-1α和caspase-9的作用

目的:探讨HIF-1α和caspase-9表达与高眼压视网膜损伤的关系。方法:大鼠60只随机分为6组,每组10只20眼。分别为假手术对照组;高眼压3,7,14,21,28d组。巩膜静脉烧烙法制作高眼压模型。应用免疫组织化学法,RT-PCR法,Western印迹法检测各组视网膜组织中HIF-1α和caspase-9基因mRNA及蛋白表达。结果:HIF-1α和casepase-9阳性染色主要位于视网膜内层即视网膜节细胞层和内颗粒层。HIF-1α和caspase-9mRNA和蛋白在正常视网膜中有低浓度的表达,高眼压3d后,表达明显上升,HIF-1α到7d时达到高峰,caspase-9到14d达到高峰,随后有所下降,但仍明显高于正常组的表达水平,差异有统计学意义。结论:HIF-1α和caspase-9是青光眼神经节细胞凋亡的发生和进展中重要的病理生理机制。     

氨基胍对大鼠慢性高眼压视网膜PI-3K表达的影响

目的研究慢性高眼压过程中大鼠视网膜磷脂酰肌醇-3-激酶（PI-3K）表达的变化及应用氨基胍对其表达的影响，探讨氨基胍对慢性高眼压视网膜的保护作用。方法应用免疫组织化学、RT-PCR和Westernblot的方法，观察应用及未应用氨基胍的慢性高眼压大鼠视网膜在不同时点的差异及PI-3K表达的变化。结果与正常对照组相比，慢性高眼压大鼠应用与未应用氨基胍者，视网膜均随着高眼压时间的延长逐渐出现形态学变化，于高眼压的第21d视网膜变薄，节细胞数量减少；在此过程中，PI-3K表达增多。慢性高眼压大鼠的视网膜应用氨基胍者与未应用氨基胍者相比，其形态学变化较小，而PI-3K表达则明显增多，两者差异具有统计学意义（P〈0．01）。结论PI-3K是慢性高眼压视网膜损伤过程中的保护性因素，氨基胍通过上调其表达发挥对视网膜的保护作用。     

Expression of Nogo-A on the retina in rat model with chronic ocular hypertension

AIM: To study the expressive variation of Nogo-A on rat retina in the process of chronic ocular hypertension. METHODS: Thirty-six healthy adult male Wistars were randomly divided into control group (6 rats) and chronic hypertension group (30 rats). Chronic hypertension was created by cauterizing the superficial scleral veins. Immunohistochemistry technique was used to evaluate the expressive varieties of Nogo-A at different time points during the course of chronic ocular hypertension. RESULTS: The success of the model was indicated by over 40% of increase in the IOP as compared with normal rats. Compared with control group, as time passed chronic hypertension group gradually had detectable morphology changes in the retina. At the 21st day of chronic ocular hypertension, retinas became thinner and the quantity of retinal ganglion cells (RGC) decreased (P<0.05). Assoicated with the morphological changes, the expression of Nogo-A was strongly increased (P<0.05). CONCLUSION: Myelin associated protein Nogo-A plays a part in the process of chronic ocular hypertension.     

大鼠慢性高眼压视网膜Nogo-A的表达

目的:研究慢性高眼压大鼠视网膜髓鞘相关抑制蛋白No-go-A表达的变化。方法:成年雄性Wistar大鼠36只随机分为正常对照组6只和慢性高眼压组30只,应用免疫组织化学方法观察慢性高眼压大鼠视网膜不同时点Nogo-A表达的变化。结果:与正常对照组相比,慢性高眼压21d大鼠视网膜变薄,节细胞数量减少(P<0.05);Nogo-A表达增多,与形态学变化相一致(P<0.05)。结论:髓鞘相关抑制蛋白Nogo-A在慢性高眼压大鼠视网膜损伤过程中发挥了重要作用。     

Diabetes has an additive effect on neural apoptosis in rat retina with chronically elevated intraocular pressure

PURPOSE: Diabetes mellitus (DM) is a risk factor for open-angle glaucoma, although the mechanistic interrelationship of the two is debatable. The purpose of this study is to test whether DM augments neural apoptosis in rat retina with chronically elevated intraocular pressure (IOP). METHODS: Sprague-Dawley rats were made diabetic by intraperitoneal injection of streptozotocin (STZ). At one month after STZ injection, three episcleral veins in one eye were cauterized to elevate IOP. Rats without STZ injection were treated likewise as diabetic controls. At 2 weeks, 1 month, and 2 months after cauterization, the retina was dissected, flat-mounted, and subjected to terminal dUTP nick end labeling (TUNEL) staining. TUNEL positive cells per unit area of the whole retina were measured. RESULTS: DM did not affect base line IOP or augment IOP elevation due to episcleral vein cauterization. TUNEL positive cells, which primarily consisted of the neurons and glial cells in the inner retina including retinal ganglion cell (RGC), were counted consistently eight times more in the diabetic retina without IOP elevation than diabetic controls (n = 9, p < 0.001). The cauterization significantly elevated IOP up to 28.9 mmHg (p < 0.001), which was reduced over time, and substantially induced apoptosis in a IOP-dependent fashion (p < 0.001). Ocular hypertensive retinas with DM had significantly more TUNEL positive cells than those without DM despite of the similar time course of IOP changes (p < 0.001). CONCLUSIONS: DM has an additive effect on apoptosis induction by chronic elevation of IOP. Diabetes may act as a risk factor of open-angle glaucoma by increasing susceptibility of retinal cells including retinal ganglion cells to apoptosis triggered by additional stresses such as elevated IOP.     

Influence of geranylgeranylacetone on the expression of HSP70 in retina of rats with chronic IOP elevation

AIM: To study the effects of geranylgeranylacetone (GGA) on the expression of heat shock protein70 (HSP70) on retinal ganglion cells (RGC) in rats with chronic intraocular pressure (IOP) elevation. · METHODS: Seventy Wistars were divided into blank control group (10 rats), chronic hypertension group (30 rats) and GGA group (30 rats). Chronic hypertension was created by cauterizing the superficial scleral veins. 800mg/kg/d GGA was given by oral daily after cauterization. Immunohis- tochemistry was used respectively to observe the changes of expression of HSP70 in the model rats and GGA interference rats at different time points during the course of chronic IOP elevation. · RESULTS: The successful model was identified as the IOP over 40% of normal rats. The retinal thickness was significantly reduced in model group and model+GGA group compared with normal rats from 21 days through 28 days after cauterization (P <0.05), and that of model rats was obviously decreased in comparison with model+GGA rats (P < 0.05). The number of ganglion cells was significantly decreased in model rats and model+GGA rats compared with normal rats from 21 days and 28 days. The stronger expression intensity (IOD) value was seen for HSP70 in the model+GGA rats by immunochemistry (P <0.01). · CONCLUSION: Systemic administration of GGA protects retina from chronic IOP elevation by regulating the expression of HSP70.     

Effect of aminoguanidine on caspase-3 expression in rat retina after ischemia-reperfusion injury

AIM: To investigate the effect of aminoguanidine(AG) on the expression of caspase-3 in rat retina after ischemia- reperfusion injury. METHODS: The rats were anesthetized with 30mg/kg sodium pentobarbital introperitoneal(ip) injections. After topical application of 10g/L dicaine,the anterior chamber was punctured with a 5-gauge needle connected to a bottle containing normal saline. Intraocular pressure was raised to 100 mmHg by elevating the saline container. The infusion needle was removed from the anterior chamber 60 minutes later. Reperfusion of the retinal vasculature was confirmed by fundus examination. AG 100mg/kg was ip injected in drug group. The rats were then euthanatized at 6, 24, and 72 hours after reperfusion, and their eyes were enucleated for immunohistochemistry. RESULTS: No specific staining was detected by using the caspase-3 antibody in the retina of control group. In ischemia group, the protein of caspase-3 was over-expressed at 6 hours and relieved at 24 hours and 72 hours, while with drug treatment, the expression of protein of caspase-3 was decreased at each time point. CONCLUSION: AG provides retinal protection against ischemia-reperfusion injury in rat retina, probably through an inducible NOS-dependent mechanism.     

替普瑞酮对大鼠慢性高眼压视网膜HSP70表达的影响

目的:研究慢性高眼压大鼠视网膜HSP70表达的变化及替普瑞酮的影响。方法:Wistar大鼠70只随机分为3组:空白对照组10只;慢性高眼压模型组30只;慢性高眼压模型+GGA组30只。采用烧灼巩膜浅层静脉的方法制备大鼠慢性高眼压模型。模型成功后给予替普瑞酮800mg/(kg.d)每日灌胃。应用免疫组织化学方法观察应用及未应用替普瑞酮的慢性高眼压大鼠视网膜不同时点的差异及HSP70表达的变化。结果:平均眼压高于正常眼压40%的手术眼为造模成功。与正常对照组相比,慢性高眼压大鼠应用与未应用替普瑞酮者,视网膜均随着高眼压时间的延长逐渐出现形态学变化,于高眼压的21d和28d视网膜变薄,节细胞数量减少;在此过程中,HSP70表达增多。慢性高眼压大鼠视网膜应用替普瑞酮者与未应用提普瑞酮者相比,其形态学变化较小,而HSP70表达则明显增多,两者差异具有统计学意义(P<0.01)。结论:替普瑞酮通过上调HSP70表达发挥对慢性高眼压视网膜的保护作用。     

Chronology of optic nerve head and retinal responses to elevated intraocular pressure

PURPOSE: To determine the chronology of optic nerve head and retinal responses to elevated intraocular pressure (IOP). METHODS: After 1 to 39 days of unilaterally elevated IOP, experimental and fellow rat eyes were examined for morphology and immunohistochemical labeling alterations and for ganglion cell DNA fragmentation. RESULTS: Mean IOP for the experimental eyes was 36 +/- 8 mm Hg, an approximately 15-mm Hg elevation above normal values. By 7 days of pressure elevation above 40 mm Hg, endogenous immunostaining for brain-derived neurotrophic factor and neurotrophin 4/5 was absent from the nerve head and superior retina, whereas normal labeling was present in the inferior retina and distal optic nerve of these same eyes. These changes were preceded by a loss of gap junctional connexin43 labeling and astrocytic proliferation in the nerve head and by increased retinal ganglion cell layer apoptosis in the retina. Nerve head depletion of neurotrophins coincided with evidence of axonal degeneration, loss of astrocytic glial fibrillary acidic protein staining, and spread of collagen VI vascular immunolabeling. After longer durations at these same pressures, neurotrophin labeling returned to nerve head glia and scattered retinal ganglion cells. CONCLUSIONS: Optic nerve head and retinal responses, including the depletion of endogenous neurotrophins, are readily identified in the rat eye after experimental IOP elevation. However, the apparent chronology of these responses suggests that the withdrawal of neurotrophic support was not the only determinant of retinal ganglion cell apoptosis and axonal degeneration in response to pressure.     

Optic nerve dynein motor protein distribution changes with intraocular pressure elevation in a rat model of glaucoma

Acute intraocular pressure (IOP) elevation causes accumulation of retrogradely-transported brain derived neurotrophic factor and its receptor at the optic nerve head (ONH) in rats and monkeys. Obstruction of axonal transport may therefore be involved in glaucoma pathogenesis, but it is unknown if obstruction is specific to certain transported factors or represents a generalized failure of retrograde axonal transport. The dynein motor complex mediates retrograde axonal transport in retinal ganglion cells (RGC). Our hypothesis was that elevated IOP interferes with dynein-mediated axonal transport. We studied the distribution of dynein subunits in the retina and optic nerve after acute and chronic experimental IOP elevation in the rat. IOP was elevated unilaterally in 54 rats. Dynein subunit distribution was compared in treated and control eyes by immunohistochemistry and Western blotting at 1 day (n=12), 3 days (n=4), 1 week (n=15), 2 weeks (n=12) and 4 weeks (n=11). For immunohistochemistry, sections through the ONH were probed with an anti-dynein heavy chain (HC) antibody and graded semi-quantitatively by masked observers. Other freshly enucleated eyes were microdissected for separate Western blot quantification of dynein intermediate complex (IC) in myelinated and unmyelinated optic nerve, ONH and retina. Immunohistochemistry showed accumulation of dynein HC at the ONH in IOP elevation eyes compared to controls (P<0.001, Wilcoxon paired sign-rank test, n=29). ONH dynein IC was elevated by 46.5% in chronic IOP elevation eyes compared to controls by Western blotting (P<0.001, 95% CI=25.9% to 67.8%, n=17). The maximum increase in ONH dynein IC was 78.7% after 1 week (P<0.05, n=5), but significant increases were also detected after 4 h and 4 weeks of IOP elevation (P<0.05, n=4 rats per group). Total retinal dynein IC was increased by 8.7% in chronic IOP elevation eyes compared to controls (P<0.03, 95% CI 1.4% to 16.1%, n=24). In the retina, IOP elevation particularly affected the 72 kD subunit of dynein IC, which was 100.7% higher in chronic IOP elevation eyes compared to controls (P<0.00001, 95% CI 71.0% to 130.4%, n=21). Dynein IC changes in myelinated and unmyelinated optic nerve were not significant (P>0.05). We conclude that dynein accumulates at the ONH with experimental IOP elevation in the rat, supporting the hypothesis that disrupted axonal transport in RGC may be involved in the pathogenesis of glaucoma. The effect of IOP elevation on other motor proteins deserves further investigation in the future.     

JAK/STAT pathway mediates retinal ganglion cell survival after acute ocular hypertension but not under normal conditions

Intraocular pressure (IOP) elevation is an important cause of glaucoma. Animal models of ocular hypertension have been widely used to mimic glaucoma to investigate the mechanisms underlying retinal ganglion cell (RGC) death and search for possible cure. The aim of the present study was to examine the role of JAK/STAT pathway in RGC viability in normal condition or after acute IOP elevation. Retinal explants obtained from intact or IOP-elevated eyes were firstly used to examine the effect of the JAK/STAT pathway inhibitors, AG490 and Jak Inhibitor I, on RGC viability in vitro. The role of this signal pathway was further investigated and confirmed in vivo. AG490 and Jak Inhibitor I were applied into the left eye on days 3, 9, and 15 post 2-h IOP elevation at 110mmHg. Fluorescence dye Fluorogold was used to retrogradely label surviving RGCs. Because macrophage recruitment was seen in the IOP-elevated eyes after inhibition of this pathway, clodronate liposomes were used to remove phagocytic cells in the eye and examine the role of JAK/STAT pathway in RGC survival independent of macrophages. Activities and location of JAK/STAT pathway in the retina were examined using Western blotting and immunohistochemistry. We found that inhibition of JAK/STAT pathway did not affect RGC survival in the retinal explants derived from intact eye but caused RGC death in the retinal explants that were derived from IOP-elevated eye. Importantly, the detrimental effect of JAK/STAT pathway inhibition on RGC survival was also observed in vivo following acute IOP elevation, but not in intact eye. In addition, both in vitro and in vivo experiments confirmed a detrimental action of phagocytic cells following acute IOP elevation and the pathway inhibition. Compatible with what were observed in vivo, Western blotting and immunohistochemistry showed that JAK/STAT activities were not present in intact retina, but acute IOP elevation activated JAK/STAT pathway in the retina, in the regions of inner nuclear layer and ganglion cell layer, including RGCs. The IOP elevation-induced JAK/STAT activities were effectively abolished by intravitreal application of AG490. This study thus shows that (1) acute IOP elevation activates JAK/STAT pathway in RGCs, and (2) JAK/STAT pathway mediates RGC survival following IOP elevation but not under normal condition.     

水通道蛋白4在慢性高眼压模型大鼠视网膜的表达

目的:研究慢性高眼压大鼠视网膜水通道蛋白4(AQP4)表达的变化与视网膜损伤的关系。方法:通过电凝巩膜表层静脉的方法制成慢性高眼压模型。用免疫组化和RT-PCR的方法观察AQP4在高眼压过程中不同时点的表达变化,同时观察在慢性高眼压过程中大鼠视网膜的形态学变化。结果:AQP4在正常和高眼压大鼠的视网膜皆有表达,表达的部位都位于节细胞层、内丛状层、内核层、外丛状层及外核层。在高眼压大鼠的视网膜上AQP4的表达随着高眼压时间的延长而增多。HE染色的组织切片上发现,与正常对照组相比高眼压大鼠视网膜的厚度有显著变化。结论:眼压升高后AQP4表达上调,与视网膜的厚度变化密切相关。     

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。     

Characteristics of Optic Nerve Damage Induced by Chronic Intraocular Hypertension in Rat

Purpose:To set up the Sharma‘s chronic intraocular hypertension model and investigate the intraocular pressure (IOP) as well as the optic nerve damage of this model in rat.Methods :The operations of the chronic intraocular hypertension model were performed as described by Sharma in 60 male Lewis albino rats. IOP was measured using the TonoPen XL immediately after surgery and then at 5 day, 2 week or 4 week intervals. Cresyl violet staining of whole-mounted retinas was used to label retinal ganglion cells (RGCs),then RGCs were counted. Paraphenylenediamine (PPD) staining was performed in the semi-thin cross sections of optic nerve of rat, in order to know whether the axons of optic nerve were degenerated or not.Results:There were 47 rats with higher IOP after the episcleral veins cauterized in 60 rats. The ratio of elevated IOP was 78.3%. The IOPs were stable in 4 weeks. After cresyl violet staining, the RGCs loss was 11.0% and 11.3% was found in the central and peripheral retina respectively after 2 weeks of increased IOP. After 4 weeks of increased IOP, the loss of RGCs was 17% for the central retina and 24.6% for the peripheral retina. In the retinas without higher IOP, there was no loss of RGCs. PPD staining showed that optic nerve of rat with about 5.3% damage of axons located at the superior temporal region. Region of affected optic nerve 1 mm posterior to the globe by light microscope showed evidence of damaged axons with axonal swelling and myelin debris.Conclusion:Sharma‘s chronic intraocular hypertension model is a reproducible and effective glaucoma model, which mimics human glaucoma with chronically elevation IOP and induced RGCs loss and damage of optic nerve.     

负压吸引对兔眼视网膜和视神经的影响

探讨准分子激光原位角膜磨镶术(1aser in situ keratomileusis,LASIK)中眼压急剧升高对视网膜和视神经的影响。方法将LASIK术中使用的巩膜负压环置于兔眼,瞬时压力达到65mm Hg(1mm Hg=0.133kPa),分别持续30s、1min及3min,在光镜和电镜下观察负压吸引后即刻摘除的(即刻组)和2周后摘除的(修复组)兔眼视神经和视网膜组织,并与正常兔眼(对照组)进行比较。结果负压吸引30s,视神经和视网膜细胞改变轻微;负压吸引1min,部分视神经纤维改变,视网膜视细胞出现异常;负压吸引3min,神经纤维和视网膜视细胞结构明显异常。即刻组和修复组组织改变基本相同。结论LASIK术中眼压急剧升高,可导致视网膜和视神经细胞的亚细胞结构改变,且持续时间越长改变越明显。     

Microarray analysis of retinal gene expression in the DBA/2J model of glaucoma

PURPOSE: The DBA/2J mouse is a model for secondary angle-closure glaucoma, due to iris atrophy and pigment dispersion, which ultimately lead to increased intraocular pressure (IOP). The study was undertaken to correlate changes in retinal gene expression with IOP elevation by performing microarray analysis of retinal RNA from DBA/2J mice at 3 months before disease onset and at 8 months after IOP elevation. METHODS: IOP was monitored monthly in DBA/2J animals, and animals with normal (3 months) or elevated IOP (8 months) were identified. RNA was prepared from three individual retinas at each age, and the RNA was amplified and used to generate biotin-labeled probe for high-density mouse gene microarrays (U430.2; Affymetrix, Santa Clara, CA). A subset of genes was selected for confirmation by quantitative RT-PCR, by using independent retina samples from DBA/2J animals at 3, 5, and 8 months of age and compared to retinas from C57BL/6J control animals at 3 and 8 months. RESULTS: There were changes in expression of 68 genes, with 32 genes increasing and 36 genes decreasing at 8 months versus 3 months. Upregulated genes were associated with immune response, glial activation, signaling, and gene expression, whereas downregulated genes included multiple crystallin genes. Significant changes in nine upregulated genes and two downregulated genes were confirmed by quantitative RT-PCR, with some showing changes in expression by 5 months. CONCLUSIONS: DBA/2J retina shows evidence of glial activation and an immune-related response after IOP elevation, similar to what has been reported after acute elevation of IOP in other models.     

银杏内酯B联合视网膜干细胞移植对青光眼大鼠的影响及机制研究

目的：研究银杏内酯B联合干细胞移植对青光眼大鼠的影响及相关机制。

方法：实验共分为五组：正常对照组(Control)、青光眼模型组(GLA)、干细胞组(RSCs)、银杏内酯B组(GKB)与混合组(RSCs+ GKB)。眼球组织进行HE染色,TUNEL染色检测视网膜神经节细胞的凋亡,免疫印迹法(Western blot)检测Bcl-2、Bax以及Cleaved caspase-3和Cleaved caspase-9的蛋白表达水平,实时荧光定量PCR(RT-qPCR)分别检测各组组织中Bcl-2、Bax mRNA表达水平。

结果：HE染色结果显示,给予干细胞或银杏内酯B处理,减少纤维间质水肿与空泡的出现,混合组纤维间质少见水肿与空泡; 银杏内酯B联合干细胞处理后显著减少视网膜神经节细胞的凋亡,上调Bcl-2的蛋白与mRNA表达水平,并下调Bax的蛋白与mRNA表达水平、Cleaved caspase-3和Cleaved caspase-9的蛋白表达水平。

结论：银杏内酯B联合干细胞能够抑制青光眼大鼠视网膜神经节细胞的凋亡,改善青光眼,其作用机制可能与调控Bcl-2、Bax、Cleaved caspase-3和Cleaved caspase-9因子的表达有关。     

视网膜光化学损伤大鼠视紫红质基因mRNA表达水平的原位杂交技术检测

目的：研究视网膜光化学损伤状况下视紫红质基因mRNA表达水平的变化规律及其与形态学改变的关系。 方法：应用原位杂交和电镜技术对光化学损伤大鼠视网膜视紫红质基因mRNA表达情况及视网膜形态学损伤性改变进行动态观察。 结果：视紫红质mRNA原位杂交信号主要分布于视网膜光感受细胞层,尤其是其内段和外段;随连续光照时间的延续,其表达迅速下降,且先于视网膜形态学的损伤性改变;同一视网膜中,上方及后极部杂交信号的减弱较下方和周边部更为明显。 结论：视紫红质基因mRNA表达水平降低可能为光化学性视网膜损伤的早期信号。 （中华眼底病杂志,1997,13：228-230）