灯盏细辛对大鼠视神经压榨伤后视网膜神经节细胞的保护作用

目的　探讨中草药灯盏细辛对大鼠标定性视神经压榨伤所致的视网膜神经节细胞(RGC)损伤的防护和修复作用。方法　 4 2只健康SD大鼠随机均分为A组和B组。两组均用特制微型视神经夹直接夹持视神经 ,制作成单眼视神经部分压榨伤模型后 ,A组不予任何治疗 ,B组予以灯盏细辛治疗 ,直至处死动物。以上两组按致伤日至处死日动物的存活时间又分为 :A1组和B1组 (损伤后 4d) ,A2 组和B2 组 (损伤后 14d) ,A3 组和B3 组 (损伤后 2 1d) ,每组各 7只大鼠。于处死前 3d双上丘直接注射 3%快蓝标记双眼RGC。处死日行眼球摘除术后 ,将双眼全视网膜组织铺片置于荧光显微镜下 ,在距视乳头 1mm处的颞上、颞下、鼻下及鼻上 4处作荧光摄影 ,并输入计算机经图像分析仪计数RGC。计算RGC标识率 ,即 (损伤眼RGC数 /未损伤眼RGC数 )× 10 0 % ,并进行统计学分析。结果　A组大鼠中 ,A1、A2 及A3 组的RGC标识率分别为 (77 79± 7 11) %、(6 3 76± 3 79) %、(5 4 6 6±4 75 ) % ;B组大鼠中 ,B1、B2 及B3 组的RGC标识率分别为 (80 13± 12 0 3) %、(78 17± 9 19) %及(83 5 9± 12 6 1) %。A2 和A3 组分别与B2 和B3 组比较 ,差异均有非常显著意义 (t=14 10 8,36 2 0 3;P<0 0 1)。结论　大鼠标定性视神经压榨伤后用灯盏细辛治疗 ,     

大鼠视神经部分切断模型的建立和重复性评价

 目的 应用自行设计的模具制作大鼠视神经部分切断模型,并评价大鼠视神经部分切断模型的可重复性。 设计 实验研究。研究对象  15只Wistar大鼠。方法  利用模具将大鼠视神经部分切断,术后对13只大鼠行荧光金逆行标记及全视网膜拼图,使用Ret-camⅡ眼底照相观察视网膜血供情况。主要指标  观察视网膜神经节细胞（RGC）形态及分布变异。结果 视神经部分切断直接影响的视网膜与周围正常视网膜有明确分界线,标记荧光金视网膜面积比例变异系数最大值为1.85%,平均变异系数为0.67%±0.44%。Ret-camⅡ眼底照相显示视神经部分切断后,未引起视网膜供血障碍。 结论 利用新型模具器械可成功建立易于量化的重复性高的RGC继发性损伤模型。（眼科,2013,22：34-37）     

大鼠视神经钳夹伤动物模型的病理学观察

目的观察大鼠视神经钳夹伤后不同时间的病理学变化及其修复规律.方法成年S-D大鼠36只,随机等分为6组:一组为正常对照,其余均用70g压力的显微无创血管钳于右眼球后1mm处夹持视神经15s,分别于损伤后3、7、14、30、60 d取材,观察视神经轴突和视网膜神经节细胞(RGC)的形态及数目变化.结果正常大鼠视神经髓鞘完整,损伤后3 d、7 d,髓鞘疏松解体,轴突内线粒体肿胀,伤后14 d胶质细胞开始增生,伤后60 d可见到新生样轴突.正常大鼠RGC单层排列,神经纤维层(RNFL)厚度均匀,伤后3 d、7 d,RGC胞浆中线粒体肿胀明显,尼氏体减少,RNFL水肿,之后上述改变程度减轻,部分恢复.轴突数目正常为555.00±93.80(单位:个/3258.04 μm2),视乳头两侧各1mm的视网膜切片RGC数目,正常为69.75±5.38(单位:个),损伤后均逐渐减少,至60 d时稍增多.结论夹持大鼠视神经70 g压力15 s可造成中等程度的损伤,表现在轴突和RGC的形态异常及数目减少,改变随时间加重,至1个月左右开始恢复.     

蛇毒神经生长因子对大鼠视神经夹伤保护的电镜观察

目的研究蛇毒神经生长因子在视神经损伤后对视网膜神经节细胞的保护作用。方法将Wistar大鼠40只随机分为实验对照组和实验治疗组。制作实验性视神经夹伤模型,用头部宽1mm的微型血管夹夹伤大鼠右眼视神经后,实验治疗组向伤眼玻璃体腔内注入蛇毒神经生长因子100BU(0.025mL)。实验对照组向伤眼玻璃体腔内注入0.025mL平衡盐液。于损伤后第3d、7d、14d、30d、60d取材,用透射电镜观察不同时间段各组视网膜形态学变化。结果电镜下大鼠视网膜改变:实验治疗组和对照组电镜下均可见坏死和凋亡。伤后14d,实验治疗组视网膜微管数目比实验对照组较多,排列比较整齐。结论在视神经损伤早期,蛇毒神经生长因子能减轻视神经夹伤后微管的损坏,提高视网膜神经节细胞的存活数量,对视网膜神经节细胞有明显的保护作用。     

视神经离断后坐骨神经移植修复反应的初步研究

目的建立大鼠坐骨神经支持下的视神经再生模型。方法大鼠右侧视神经离断后移植一段自身视神经或坐骨神经,分别建立视神经自身吻合模型和视神经-坐骨神经吻合模型。建立模型后第3天、第7天和第14天处死动物,处死前3d将荧光染料Dil注射到移植的神经断端,应用逆行标记的方法观察不同模型中视网膜神经节细胞(RGCs)轴突的再生情况。结果术后3d,两组均无明显的Dil标记细胞;7d后,视神经自身吻合组无明显的荧光标记细胞,视神经-坐骨神经吻合组可见明显的Dil标记细胞,细胞密度分别为(152±26)/mm2,14d后增加为(297±31)/mm2,而此时,视神经自身吻合组仅在一只大鼠的视网膜铺片上见到一Dil标记细胞。结论成功建立了坐骨神经支持下的视神经再生模型。     

两种常用大鼠视神经钳夹伤模型造模效果的比较

背景 视神经钳夹伤(ONC)动物模型是外伤性视神经损伤致病机制及治疗方法相关基础研究的主要工具,目前常用的造模方法有经眼眶上缘开神经鞘膜视神经钳夹法和经球结膜外眦部夹伤视神经法,但关于2种模型优劣评价的研究很少. 目的 比较2种常用大鼠ONC模型的造模效果,为相关的实验研究中造模方法的选择提供依据.方法 采用随机分配方法将8～10周龄健康成年雄性SD大鼠24只分为经眶上缘开神经鞘膜ONC组和经眶上缘开神经鞘膜ONC 20 s、40 s、60 s组,分别采用经眶上缘开神经鞘膜视神经夹伤法(20 s)及经球结膜外眦部夹伤视神经法在大鼠的一侧眼建立ONC动物模型,各组大鼠的正常对侧眼作为对照.于造模后14 d记录各组大鼠闪光视觉诱发电位(F-VEP)P1波;制备大鼠视神经组织切片,采用苏木精-伊红染色法观察大鼠视神经的组织病理学改变;采用免疫荧光法观察并计数大鼠视网膜组织中Brn-3α阳性视网膜神经节细胞(RGCs).对2种造模方法的造模过程和检测结果进行比较.结果 造模后14d,经眶上缘开神经鞘ONC组和经球结膜ONC 20 s组、40 s组、60 s组大鼠的F-VEP P1波潜伏期较各自的正常对侧眼均明显延长,差异均有统计学意义(t=-11.64、-8.04、-6.50、-10.84,均P＜0.01);经眶上缘开神经鞘ONC组大鼠P1波潜伏期与经球结膜ONC 20 s、40 s、60 s组大鼠比较均明显延长,差异均有统计学意义(P=0.01、0.02、0.05);各组大鼠术眼P1波振幅与其正常对侧眼比较差异均无统计学意义(均P＞0.05).造模后14 d,免疫荧光检测显示各组大鼠模型眼视网膜上Brn-3α表达阳性RGCs数均较正常对侧眼明显减少,经眶上缘开神经鞘ONC组大鼠视网膜上Brn-3α表达阳性RGCs数为(13.60±2.14)个/视野,为其正常对侧眼的47.49％,经球结膜ONC 20 s、40 s和60 s组中Brn-3α阳性RGCs数分别为(18.74±3.61)、(15.84±2.31)和(14.58±3.23)个/视野,分别为其正常对侧眼的67.70％、56.69％和50.17％,经眶上缘开神经鞘ONC组大鼠视网膜中Brn-3α阳性RGCs数与经球结膜ONC 40 s和60 s组比较,差异均无统计学意义(均P＞0.05).组织病理学检查显示,各组大鼠造模眼神经胶质细胞核排列紊乱,细胞基质空泡化,可见大量炎性细胞浸润,以眶上缘开神经鞘ONC组更为严重.结论 与经球结膜ONC模型鼠比较,经眶上缘开视神经鞘ONC模型大鼠视神经形态结构损害更为严重,视神经的传导功能更为迟缓,RGCs的存活率更低.     

大鼠外伤性视神经损伤模型的建立

目的建立大鼠定量视神经损伤模型,为研究视神经损伤的发病机制及治疗效果奠定基础。方法健康Sprague-Dawley大鼠27只,随机分为3组,分别为A组(损伤组)12只、B组(假损伤对照组)12只、C组(正常对照组)3只。A组暴露视神经,应用40g力的视神经夹在大鼠眼球后2mm处夹视神经30s,B组仅暴露视神经,C组不做任何处理。A、B组按损伤后不同时间分为3d组、7d组、14d组、28d组,采用双上丘注射50g.L-1荧光金标记双眼视网膜神经节细胞(retinal ganglion cells RGCs)。视网膜铺片荧光照相,计算RGCs计数,RGCs标识率及RGCs丧失率。结果 C组与B组RGCs计数及RGCs标识率比较,无明显差异;A组与B组各时间点RGCs计数及RGCs标识率比较,均有明显差异;A组视神经损伤后不同时间RCCs计数逐渐下降(3d:152.26±25.12,7d:111.19±20.32,14d:101.23±17.19,28d:94.86±18.26),14d组与28d组比较无统计学意义,其他时间点比较有统计学意义,视神经损伤后RGCs标识率随时间延长渐进性降低(3d:79.35%±8.29%,7d:59.76%±7.79%,14d:53.26%±7.26%,28d:51.29%±3.26%),而RGCs丧失率随时间延长渐进性增加(3d:20.65%±3.15%,7d:40.24%±5.63%,14d:46.74%±4.37%,28d:48.71%±5.12%)。结论应用40g力视神经夹在大鼠眼球后2mm处夹视神经30s能成功建立定量视神经损伤动物模型。     

兔视神经挫伤的实验研究

目的 研究兔视神经挫伤后视网膜、视神经结构及功能变化.方法 建立兔视神经挫伤模型,于不同时间作视网膜节细胞(RGC)、轴突染色记数,并检测闪光视诱发电位(FVEP).结果 伤后RGC数目持续下降并伴有轴突变性、坏死,4周时RGC平均记数为12.67±4.12/mm,轴突密度为36,085±285/mm2,均明显少于正常对照(P＜0.01).在伤后4小时FVEP下降至对照眼的54%,并持续至8周.结论 兔视神经挫伤后RGC、视神经出现渐进性退变,伴有视神经功能即刻下降.     

天麻钩藤饮抗大鼠视神经夹伤模型视网膜神经节细胞凋亡作用的实验研究

目的 观察天麻钩藤饮对视神经夹伤模型大鼠视网膜神经上皮层厚度和视网膜神经节细胞（RGC）凋亡的影响。设计 实验研究。研究对象 SPF级雄性Wistar大鼠48只。方法 将大鼠随机分6组,每组8只,分别为正常对照组,阴性对照组,天麻钩藤饮低剂量组（0.6 g/ml）、中剂量组（1.2 g/ml）、高剂量组（2.4 g/ml）和银杏叶片阳性对照组（1.2 mg/ml）,除正常对照组大鼠不做处理,其他组大鼠右眼均建立视神经夹伤模型,正常对照组和阴性对照组给予纯净水灌胃。于给药30天处死动物取眼球,做石蜡切片HE染色,观察各组视网膜神经上皮层厚度,TUNEL法检测RGC的凋亡程度。主要指标 HE染色视网膜神经上皮厚度及RGC凋亡数量。结果 阴性对照组（171.04±13.86 μm）比正常组（208.98±8.46 μm）视网膜神经上皮厚度显著减少（P=0.000）。而天麻钩藤饮中、高剂量组大鼠视网膜厚度（分别为187.68±11.16 μm 和189.22±9.54 μm）比阴性对照组显著增加（P=0.043,0.001）,且中、高剂量组与阳性对照组（191.35±9.03 μm）之间无显著差异（P=0.052,0.670）;TUNEL凋亡检测发现,阴性对照组凋亡细胞数（9.09±2.24个/高倍视野）比正常组（0.59±0.61个/高倍视野）明显增加（P=0.000）,中剂量组、高剂量组和阳性对照组RGC的凋亡（分别为7.00±1.88, 5.22±2.05, 5.03±2.03个/高倍视野）均比阴性对照组显著减少（P=0.024, 0.000,0.000）。结论 天麻钩藤饮对大鼠视神经夹伤模型具有一定抗RGC凋亡的作用,随药物浓度的升高,抗凋亡作用更显著。     

视神经鞘切开减压术对大鼠视神经挤压伤后RGC凋亡的影响

目地观察早期视神经鞘切开减压术对大鼠视神经挤压伤后RGC凋亡的相关机制。方法大鼠91只分为对照组、损伤组、手术组各7、42、42只通过视网膜切片技术,HE染色,免疫组化SP法于伤后3、7、15各时问点视网膜神经节细胞计数及检测BCL-2和BAX阳性细胞数。结果手术组各时间点RGC计数均高于损伤组,差异有显著性（P〈0．05）。手术组各时间点BCL-2阳性细胞数均高于损伤组,BAX阳性细胞数均低于损伤组,差异有显著性（P〈0．05）。结论早期视神经鞘切开减压术可对大鼠视神经挤压伤后能上调BCL-2基因的表达和下调BAX基因的表达而抑制RGC的凋亡。     

The Protective Role of Mecobalamin Following Optic Nerve Crush in Adult Rats

IntroductionProgressivelossofganglioncellsandtheiraxonsisafeatureofoculardiseasessuchasopticnervedamage,glaucoma,ischemia,andinfla鄄mmation.Thelossofganglioncellsaffectsbothopticnervefibersandtheirsheaths.Thisresultsinalossofneuralnutritionandalossofbloodandoxygensupplythatcanleadtotheaccum鄄ulationofextracellularglutamateresultinginexcitoxitywhichinfluencestheconductionofvisualelectricsignals.Thesetwofactorsresultinapoptosisofretinalganglioncells[1].Furthermore,degenerationcontinuestoprogres…     

Sigma-1R Protects Retinal Ganglion Cells in Optic Nerve Crush Model for Glaucoma

PurposeThe purpose of this study was to determine the effects of the Sigma-1R (σ-1r) on retinal ganglion cell (RGC) survival following optic nerve crush (ONC) and the signaling mechanism involved in the σ-1r protection.MethodsThe overall strategy was to induce injury by ONC and mitigate RGC death by increasing σ-1r expression and/or activate σ-1r activity in σ-1r K/O mice and wild type (WT) mice. AAV2-σ-1r vector was used to increase σ-1r expression and σ-1r agonist used to activate the σ-1r and RGCs were counted. Immunohistochemical and Western blot analysis determined phosphorylated (p)-c-Jun, c-Jun, and Caspase-3. Pattern electroretinography (PERG) determined RGC activity.ResultsRGC counts and function were similar in pentazocine-treated WT mice when compared to untreated mice and in WT mice when compared with σ-1r K/O mice. Pentazocine-induced effects and the effects of σ-1r K/O were only observable after ONC. ONC resulted in decreased RGC counts and activity in both WT and σ-1r K/O mice, with σ-1r K/O mice experiencing significant decreases compared with WT mice. The σ-1r transgenic expression resulted in increased RGC counts and activity following ONC. In WT mice, treatment with σ-1r agonist pentazocine resulted in increased RGC counts and increased activity when compared with untreated WT mice. There were time-dependent increases in c-jun, p-c-jun, and caspase-3 expression in ONC mice that were mitigated with pentazocine-treatment.ConclusionsThese findings suggest that the apoptotic pathway is involved in RGC losses seen in an ONC model. The σ-1r offers neuroprotection, as activation and/or transgenic expression of σ-1r attenuated the apoptotic pathway and restored RGCs number and function following ONC.     

Chronic Human Glaucoma Causing Selectively Greater Loss of Large Optic Nerve Fibers

Eighteen eyes of 12 persons with chronically elevated intraocular pressure (IOP) were studied histologically to determine the number and diameter of optic nerve fibers. In some eyes, automated perimetry had been performed. Optic nerve fibers larger than the mean diameter were killed more rapidly than smaller fibers, although no fiber size was completely spared at any stage of atrophy. The number of optic nerve fibers varies considerably among normal eyes. The authors confirmed that the death of a substantial proportion of optic nerve fibers precedes detectable visual field loss.     

小鼠视神经损伤后视神经小胶质细胞数目和形态变化

目的：研究小鼠视神经损伤后不同时间点视神经小胶质细胞的数目与形态变化。方法：实验研究。选取32只成年雄性健康CX3CR1—/GFP转基因杂交小鼠,按照随机数字表法将小鼠随机分为正常对照组、视神经损伤1、7、14 d组,每组8只。视神经损伤组均在左眼建立视神经夹伤模型,右眼不处理,正常对照组不做任何处理。分别于上述时间点制备小鼠视神经冰冻切片,每根视神经取3张切片（30 μm）,采用共聚焦显微镜在距离眼球端500 μm处拍摄图像,比较小胶质细胞的数量和形态变化。4组小胶质细胞数目比较采用单因素方差分析。结果：正常对照组、视神经损伤1、7和14 d组的视神经小胶质细胞数目分别为（438±16）个/mm2、（323±15）个/mm2、（1 252±107）个/mm2、（1 474±113）个/mm2。视神经损伤7、14 d组小胶质细胞数量明显多于正常对照组和视神经损伤1 d组,差异均有统计学意义（均 P<0.001）。正常对照组的视神经小胶质细胞均匀分布,细胞核较小,分枝细长并向四周伸展。视神经损伤1 d组,小胶质细胞分枝数量减少,细胞核形态变化不明显。损伤7 d组的视神经小胶质细胞大量激活,排列较紊乱,存在少量细胞聚集现象,分枝短而粗,且越靠近细胞核分枝越粗,细胞核体积明显增大。视神经损伤14 d组,视神经小胶质细胞形态与损伤7 d组类似。结论：小鼠视神经夹持损伤后,视神经小胶质细胞初期数目减少,随着损伤时间延长,小胶质细胞数目大量增加,且形 态由分枝状变为阿米巴样。     

Optic Nerve Engraftment of Neural Stem Cells

PurposeTo evaluate the integrative potential of neural stem cells (NSCs) with the visual system and characterize effects on the survival and axonal regeneration of axotomized retinal ganglion cells (RGCs).MethodsFor in vitro studies, primary, postnatal rat RGCs were directly cocultured with human NSCs or cultured in NSC-conditioned media before their survival and neurite outgrowth were assessed. For in vivo studies, human NSCs were transplanted into the transected rat optic nerve, and immunohistology of the retina and optic nerve was performed to evaluate RGC survival, RGC axon regeneration, and NSC integration with the injured visual system.ResultsIncreased neurite outgrowth was observed in RGCs directly cocultured with NSCs. NSC-conditioned media demonstrated a dose-dependent effect on RGC survival and neurite outgrowth in culture. NSCs grafted into the lesioned optic nerve modestly improved RGC survival following an optic nerve transection (593 ± 164 RGCs/mm² vs. 199 ± 58 RGCs/mm²; P < 0.01). Additionally, RGC axonal regeneration following an optic nerve transection was modestly enhanced by NSCs transplanted at the lesion site (61.6 ± 8.5 axons vs. 40.3 ± 9.1 axons, P < 0.05). Transplanted NSCs also differentiated into neurons, received synaptic inputs from regenerating RGC axons, and extended axons along the transected optic nerve to incorporate with the visual system.ConclusionsHuman NSCs promote the modest survival and axonal regeneration of axotomized RGCs that is partially mediated by diffusible NSC-derived factors. Additionally, NSCs integrate with the injured optic nerve and have the potential to form neuronal relays to restore retinofugal connections.     

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.     

Effect of High Dosage of Methylprednisolone on Rat Retinal Ganglion Cell Apoptosis after Optic Nerve Crush

Traumaticopticneuropathyisanuncommonbutoftendevastatingcauseofpermanentvisuallossafterbluntorpenetratinginjury.Opticnerveiscomposedoftheaxonsofretinalganglioncells(RGC).Opticnerveaxotomycausedrapiddegenerationoftheaxonsandmorethan90%oftheRGCdiedbyapoptosiswithin2weeks[1].AttemptsweremadetopreservetheinjuriedRGCbychangingtheenvironmentorbyupregulatingintrinsicgrowthfactorssurroundingtheRGC[2].Apoptosisisaregulatedprocessunderthecontrolofproteins.TheBcl鄄2genefamilyisoneofthemostimportanta…     

Histopathological Changes of Inner Retina,Optic Disc,and Optic Nerve in Rabbit with Advanced Retinitis Pigmentosa

We observed the histopathological changes of retinal ganglion cells (RGCs), optic disc, and optic nerve in rabbit with advanced retinitis pigmentosa (RP). Wild-type (WT) and rhodopsin transgenic (Tg) of RP rabbits were used at age 24 months. Light and electron microscopy were used to observe the retina, optic disc, and optic nerve. RGCs were also confirmed by immunofluorescent staining with a TUJ-1 monoclonal antibody. In addition to the rod and cone degeneration, we observed the astrocyte infiltration of the optic disc due to the damage of small RGCs and nerve fibres and atrophy of small optic nerve fibres. They subsequently lead to the optic disc excavation and atrophy of the optic nerve. Consequently, our histopathological study clarified that not only the outer retina but also the inner retina, the optic disc, and the optic nerve were also affected in the late stages of RP rabbit.     

The effect of ginkgo biloba on the rat retinal ganglion cell survival in the optic nerve crush model

Purpose: To investigate the effect of ginkgo biloba on the retinal ganglion cell survival in a rat optic nerve crush model. Methods: Twenty‐four Sprague–Dawley rats were divided randomly into a study group of 12 animals receiving intraperitoneal injections of ginkgo biloba and a control group of 12 animals receiving intraperitoneal saline injections. All injections were performed 1 hr before the optic nerve crush and daily afterwards. For each animal, the right optic nerve was crushed closely behind the globe for 60 seconds using a microclip with 40 g power. The left optic nerve was kept intact. At 23 days after the optic nerve crush, the retinal ganglion cells were labelled retrogradely by injecting 3% fluorogold into both sides of the superior colliculus of the brain. At 4 weeks after the optic nerve crush, the animals were killed. Photographs taken from retinal flat mounts were assessed for the number and density of the retinal ganglion cells. Results: The survival rate, defined as the ratio of the retinal ganglion cell density in the right eye with the optic nerve crush divided by the retinal ganglion cell density in left eye without an optic nerve trauma, was significantly (p = 0.035) higher in the study group with ginkgo biloba than in the control group (60.0 ± 6.0% versus 53.5 ± 8.0%). Conclusion: The results suggest that intraperitoneal injections of a ginkgo biloba extract given prior to and daily after an experimental and standardized optic nerve crush in rats were associated with a higher survival rate of retinal ganglion cells.