维拉帕米对大鼠视网膜光损伤的防护作用

目的 寻找有效、方便的药物以防护光性视网膜损伤。方法 选用维拉帕米作为防护剂，于光损伤后即刻，４、１５及３０天分别检测损伤组与防护组大鼠视网膜组织内脂质过氧化终产物丙二醛（ＭＤＡ）的含量及组织病理结构。并观察血－视网膜外屏障的完整性。结果正常视网膜内ＭＤＡ含量为０．３６±０．０７ｎｍｏｌ／ｍｇ，损伤组各不同时间点含量为０．５２±０．０３ｎｍｏｌ／ｍｇ、０．７０±０．２０ｎｍｏｌ／ｍｇ、０．５２±     

枸杞多糖对大鼠视网膜光损伤的形态及功能的影响

目的探讨枸杞多糖（LBP）对视网膜光损伤形态及功能的影响。设计实验性对照研究。研究对象SD大鼠60只,每组10只。方法建立视网膜光损伤模型,未治疗组于光照前、光照后1天、6天及14天行暗视闪光视网膜电图（ERG）检查,检查完后取每组大鼠眼球上方中央部视网膜行组织病理学检查。于光照前24h及0．5h腹腔注射LBP和生理盐水分别作为LBP治疗组及阳性对照组,光照后1天行暗视闪光ERG,后取眼球上方中央部视网膜标本行组织病理学检查。主要指标ERGb波振幅,视网膜形态学。结果在未治疗组,光照后各时间点标本与正常组对比ERGb波振幅明显下降,第1天降至29．97％,而第6天、第14天b波振幅无继续下降。第1天标本组织形态学显示其损伤最严重,第6天、第14天标本形态上则慢慢恢复。LBP治疗组,ERGb波振幅较阳性对照组明显升高（P=0．005）,视网膜形态学未见明显凋亡改变。结论LBP对大鼠视网膜光损伤的功能和形态损害具有防护作用。（眼科,2009,18：229-233）     

多焦视网膜电图在大鼠视网膜光损伤模型评价中的应用

目的 观察大鼠视网膜光损伤多焦视网膜电图(multifocal electroretinogram,mfERG)的改变,探讨运用mfERG对动物模型进行评价及其在药物开发研究中的价值.方法 采用自制光照箱维持光照24 h以建立大鼠视网膜光损伤模型,将模型动物随机分为4组,分别为模型对照组(光照后即刻),光照后3 d、7 d和14 d组,另设正常对照组,每组10只.按标准刺激和记录方法,分别记录各组大鼠mfERG波形的改变.结果 模型对照组与正常对照组比较,mfERG的N1及P1波各环反应密度均明显减弱,N1波(1～5环)反应密度为(6.23±3.77)nV·deg-2～(0.95±1.18)nV·deg-2,正常对照组为(47.87±12.78)nV·deg-1～(8.16±5.26)nV·deg-2,二者比较差异有显著统计学意义(P<0.01),P1波(1～5环)反应密度为(28.25±15.18)nV·deg-2～(9.18±3.18)nV·deg-2,正常对照组为(118.43±20.58)nV·deg-2～(39.27±8.44)nV·deg-2,二者比较差异有显著统计学意义(P<0.01).光照后3 d、7 d和14 d后有不同程度恢复,与模型对照组比较差异有统计学意义(P均<0.05),但仍未恢复至正常水平;N1波各环峰潜时在光照前后无明显改变(P>0.05);P1波各环峰潜时光照后与模型对照组比较显著延迟(P<0.05),但14 d后各环峰潜时已基本恢复正常(P>0.05).结论 mfERG能较好地反映光损伤大鼠视功能的损伤程度,为客观评价模型动物视功能损害提供了量化方法,可用于药物开发研究中的药效学评价.     

中药黄斑颗粒灌胃对大鼠视网膜光损伤细胞凋亡的影响

目的:观察中药复方黄斑颗粒对大鼠视网膜光损伤细胞凋亡的影响。方法:雄性SD大鼠21只分为给药组、对照组和正常组,光损伤前10d用中药复方黄斑颗粒灌胃,对照组用等体积蒸馏水灌胃,正常对照组正常饲养。光损伤白色荧光灯平均光照强度2800Lux,暗适应24h后,散瞳光照5h后置暗环境饲养,光损伤后继续给药给水,3d后取眼球做石蜡包埋切片,用TUNEL方法进行染色,同时留取眼球进行电镜观察超微形态改变。结果:正常组视网膜结构规整,几乎无TUNEL染色阳性细胞,对照组外核层有大量黄色阳性细胞,结构紊乱,给药组散在少量阳性细胞;电镜下观察可见对照组色素上皮细胞微绒毛消失,光感受器外段排列紊乱,外核层有较多的固缩凋亡细胞核,而给药组则散在少量凋亡细胞。结论:中药黄斑颗粒可能通过对抗细胞凋亡而对大鼠视网膜光损伤起到保护作用。     

光损伤对大鼠血-视网膜屏障功能的影响

目的：探讨强光对大鼠血－视网膜屏障功能的影响。方法：大鼠随机分为光照组及对照组,光照组大鼠经散瞳后进行10000lx强光照射（12h光照,12h避光,连续1～14d）,对照组只接受自然光线照射。分别于强光照射后第1、3、7、14 d 摘除相应的光照组和对照组大鼠双侧眼球;并用HE染色观察视网膜各层结构变化,用电镜观察视网膜超微结构变化,用伊凡思蓝（Evans blue,EB）灌注后激光共聚焦显微镜下微循环成像及分光光度法定量检测视网膜微循环通透性变化,来评估血－视网膜屏障变化。结果：大鼠在强光照射1d后就出现视网膜光感受器细胞变性、外节膜盘脱落、外核层厚度变薄等超微结构改变,并随着强光照射持续而逐渐加重,3 d后出现光感受器细胞凋亡,至14 d时外核层厚度已明显变薄、细胞数也明显减少。大鼠在强光照射1 d后视网膜血管就出现EB染料渗漏,至14 d时EB染料渗漏最明显。结论：强光照射可导致大鼠视网膜外核层光感受器细胞变性、凋亡,外核层厚度变薄、细胞数减少,血－视网膜屏障结构、功能破坏。     

岩茶提取物对大鼠视网膜光损伤的保护作用

目的　探讨岩茶提取物对大鼠视网膜光损伤的保护作用。方法　４０只ＳＤ大鼠随机分为４组:正常对照组、光损伤组、高剂量组（０．２０ｇ?Ｌ－１）和低剂量组（０．０５ｇ?Ｌ－１）。除正常对照组外,其余三组置于光照强度为（４０００±２００）Ｌｕｘ的光照箱内照射１２ｈ。高、低剂量组光照前３ｄ给予岩茶提取物尾静脉注射,每天一次,光照结束后继续给药７ｄ后处死。光镜下观察４组视网膜病理变化,检测视网膜组织外核层厚度、超氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ,ＳＯＤ）活力及丙二醛（ｍａｌｏｎａｌｄｅｈｙｄｅ,ＭＤＡ）含量。结果　光损伤组光镜下视网膜各层结构疏松,外核层厚度变薄,见大量空泡细胞;感光细胞内外节排列紊乱,染色不均。高、低剂量组损伤均较光损伤组轻,其中高剂量组损伤更轻。与正常对照组（４１．０６±１．０１）μｍ比较,其余三组视网膜外核层厚度变薄（均为Ｐ＜０．０５）,高、低剂量组较光损伤组（１５．１０±１．９２）μｍ厚,其中高剂量组（２５．７７±１．０８）μｍ较低剂量组（１９．２４±０．５５）μｍ厚（Ｐ＜０．０５）。与正常对照组相比,其余三组视网膜组织ＳＯＤ活力下降（Ｐ＜０．０５）,ＭＤＡ含量升高（Ｐ＜０．０５）;与光损伤组比较,高、低剂量组视网膜ＳＯＤ活力升高（Ｐ＜０．０５）,ＭＤＡ含量下降（Ｐ＜０．０５）,高剂量组表现更明显（Ｐ＜０．０５）。结论　岩茶提取物对大鼠视网膜光损伤有一定的保护作用,且具有剂量依赖性。     

明目"五子"对大鼠光损伤视网膜一氧化氮水平的影响

目的观察中药明目"五子"对大鼠光损伤视网膜一氧化氮(NO)水平的影响,并探讨其对视网膜光损伤的保护作用及其机制.方法采用绿色荧光灯持续照射24 h造成大鼠视网膜光损伤.同时分别给予中药明目"五子"高、低剂量灌胃,连续给药14 d后,采用硝酸还原酶法检测视网膜NO的含量.结果光照后,大鼠视网膜NO含量升高;"五子"高、低剂量组能降低视网膜NO的含量,与模型对照组比较差异有显著性(P<0.05～0.01).结论明目"五子"可降低视网膜NO水平,减轻光对视网膜的损伤.     

色素上皮衍生因子对视网膜光损伤保护作用的体内研究

目的:探讨色素上皮衍生因子(pigment epithelium derived factor,PEDF)对光损伤的视网膜感光细胞的作用。方法:Sprague Dawley(SD)鼠右眼玻璃体腔内注射PEDF,左眼注射磷酸盐缓冲液(phosphate buffered solution,PBS)作对照。注射2d后将SD鼠置于1000~1400lx弥散白色冷荧光灯下连续光照2,5,7d后分别行ERG检查和组织学分析。结果:连续光照2,5,7d后,PEDF处理组与PBS对照组的外核层(outer nuclear layer,ONL)厚度及ERGb波振幅均呈逐渐下降趋势,统计学分析两组差别具有显著性意义(P<0.01)。结论:PEDF对光损伤的视网膜感光细胞具有保护作用。     

缺血预处理对大鼠视网膜缺血再灌注损伤保护作用

目的：探讨缺血预处理是否对视网膜缺血再灌注损伤有保护作用及其机理,方法：利用前房灌注生理盐水形成高眼压的视网膜缺血再灌注损伤的动物模型,视网膜缺血时间为1h分别于缺血前30min、24h或72h对大鼠一只眼5min短暂缺血即预处理,24h或72h后行视网膜电图（ERG）、电镜、光镜、丙二醛（MDA）及热休克蛋白70（HSP70）检测,或者一侧眼行5min假处理,24h后行1h缺血,24h或72h再行上述检测,所有对侧眼不作处理作对照,结果：与假处理相相比,缺血前24、72h进行预处理后的大鼠视网膜光镜、电镜表现损害明显减轻,ERGb波明显恢复（P＜0．01）,MDA含量降低（P＜0．01）,缺血前30min预处理的视网膜表现严重的损害,ERGb波几安全消失,结论：缺血预处理对视网膜缺血再灌注损伤有保护作用,且有一定时限性。     

视网膜光损伤的研究进展

视网膜光损伤及其损伤防御机制和药物性防治的研究一直是数十年来眼科领域一个基础结合临床的重要研究课题。本文回顾了视网膜光损伤的研究历史，从致伤光源的性能，光损伤的影响因素，分子病理机制的研究进展，及其防治措施等方面的研究进展进行综述，指出在视网膜光化学损伤过程中，存在着我种因素的调控与影响，其损伤机制是多层次多方面的，但随着分子生物学在光损伤机制研究中的普遍应用，光损伤确切的分子致病机制可在不久的将     

Protective effects of soft acrylic yellow filter against blue light-induced retinal damage in rats

Recently, a yellow intraocular lens (IOL) was developed for the purpose of reducing potential blue light-induced retinal damage after cataract surgery. However, the effect of yellow filters on retinal protection remains to be clarified. To test the protective effects of yellow filters on blue light-induced retinal damage, a yellow and a clear soft acrylic filter were attached to the right and left eyes, respectively, of albino rats and exposed to 4.5 k lux blue fluorescent lights with peak wavelength at 420 nm (ranging 380-500 nm; short blue) or 446 nm (ranging 400-540 nm; long blue) for 6h. To assess retinal damage, the electroretinogram (ERG) was recorded at 7 days, outer nuclear layer (ONL) thickness and area were measured at 7 days, apoptosis was analyzed by TUNEL staining at 24 h, and the level of lipid peroxidation in retinas was assessed by Western dot blots using specific antibodies against 4-hydroxynonenal (4-HNE)- and carboxyethylpyrrole (CEP)-modified proteins immediately after light exposure. After short blue light exposure, a- and b-wave ERG amplitudes and the ONL thickness at 1-2.5 mm inferior and 0.5-2.5 mm superior to optic nerve head (ONH) were significantly reduced. TUNEL staining in the ONL at 0-2 mm inferior and 1-2 mm superior to the ONH, and retinal levels of 4-HNE- and CEP-modified proteins were significantly increased in the clear filter-covered eyes compared to yellow filter-covered eyes. After long blue light exposure, the only difference seen was a greater ONL thickness at 1.5 mm superior to the ONH in yellow filter-covered eye. Transmission of light through the yellow filter was 58% for short blue and 89% for long blue compared to the clear filter. The ONL area was not different between clear filter-covered and -uncovered eyes after exposure to short or long blue light. Given the results, yellow IOL material protects the retina against acute shorter wavelength blue light exposure more effectively than the clear IOL material.     

枸杞子提取物对光诱导视网膜损伤的保护作用

目的探索枸杞子提取物对人视网膜色素上皮(ARPE-19)细胞及C57BL/6J小鼠视网膜光诱导损伤的保护作用。方法 ARPE-19细胞分为正常细胞对照组,光诱导细胞损伤组,细胞低、中、高剂量组(0.1 g·L^-1、0.5 g·L^-1、1.0 g·L^-1枸杞子提取物+光诱导细胞损伤),测定各组细胞活力以及细胞内活性氧(ROS)含量的变化。40只C57BL/6J小鼠随机分为正常动物对照组,光诱导动物损伤组,动物低、中、高剂量组(280 mg·kg^-1、370 mg·kg^-1、460 mg·kg^-1枸杞子提取物+光诱导动物损伤组),每组8只。各剂量枸杞子提取物干预组小鼠在6周龄开始给予枸杞子提取物灌胃,8周后再给予10 000 lux光照射24 h;光照结束后ERG评估各组小鼠视网膜功能,OCT检测视网膜外核层(ONL)厚度,FFA检测视网膜血管渗漏情况,HE染色后对视网膜ONL细胞进行计数,同时检测血清中丙二醛(MDA)含量和超氧化物歧化酶(SOD)、谷胱甘肽...     

显微白内障手术光性视网膜损伤的F—ERG观察

目的　观察现代囊外白内障术中显微镜光照对视网膜功能的影响。方法　应用国际标准化视网膜电流图(F-ERG)记录45例45眼白内障术前及(白内障囊外摘出)术后1moF-ERG最大反应(MCR)(a、b波振幅)。按(WHO)晶状体混浊度分级采用不同术式,A组PHACO术、B组ECCE术。A组术中实际曝光于显微镜下25～40min(31.4min±4.1min),中度光强;B组50～75min(59.8min±8.7min),中高度光强。比较2组中使用不同显微镜光照(时间和光强)对ERG反应的影响,评价其对视网膜功能的损害。结果　白内障术后1moF-ERGa、b波振幅较术前均有不同程度的增大(0.01＜P＜0.05);A组术后F-ERG振幅较术前明显增大(P＜0.01);B组较术前增大,但无显著性差异(0.01＜P＜0.05)。结论　白内障术后ERG反应有不同程度的增强,提示晶状体混浊可减弱ERG反应;显微镜光照下手术时间越长、光照越强,术后1moF-ERG反应增幅越小,提示持续显微镜下手术可致视网膜光毒性损伤。     

熟地黄、枸杞子及其混合提取物对小鼠视网膜光损伤的保护作用

目的　探讨熟地黄、枸杞子及其混合提取物对小鼠光诱导视网膜损伤的作用。方法　雄性C57BL/6小鼠34只,随机分为5组:对照组、模型组、熟地黄组、枸杞子组、熟地黄+枸杞子组,药物干预组分别予相应药物提取物灌胃,并暴露于一定光照强度下。通过视网膜电图测量视觉功能,光学相干断层扫描观察活体视网膜形态,荧光素眼底血管造影术观察视网膜血管形态和面积,病理切片HE染色观察视网膜结构变化, TUNEL染色观察视网膜细胞凋亡情况,通过检测血液中抗氧化酶活性及丙二醛浓度评价药物抗氧化作用。结果　枸杞子组、熟地黄+枸杞子组小鼠光损伤后视网膜电图中0.01 cds?m^-2、3.00 cds?m^-2、10.00 cds?m^-2暗反应下b波波幅较模型组均提高,其中熟地黄+枸杞子组较模型组0.01 cds?m^-2暗反应震荡电位(OPS)波显著提高,差异均有统计学意义（均为P<0.05）。模型组小鼠的眼底照相中观察到视网膜渗出样改变和玻璃膜疣样病变,但在对照组、枸杞子组和熟地黄+枸杞子组中未观察到此病变。在HE染色中,模型组外核层结构有明显的紊乱、细胞密度降低趋势,对照组、熟地黄组、枸杞子组和熟地黄+枸杞子组外核层细胞排列紧密且规则。与模型组比较,枸杞子组、熟地黄组、熟地黄+枸杞子组可显著降低视网膜细胞凋亡率（均为P<0.05）。熟地黄组、枸杞子组和熟地黄+枸杞子组中超氧化物歧化酶活性较模型组分别升高了8.93%、16.30%、20.57%,熟地黄组、枸杞子组、熟地黄+枸杞子组中谷胱甘肽过氧化物酶活性较模型组分别升高了14.44%、20.05%、36.04%,熟地黄+枸杞子组中丙二醛含量较模型组降低了7.60%,差异均有统计学意义(均为P<0.05)。结论　熟地黄、枸杞子对AMD模型小鼠的视网膜功能与结构有保护作用,两种药物同时干预效果更加明显。     

Protective effect of saturated hydrogen saline against blue light-induced retinal damage in rats

AIM: To explore the effect of saturated hydrogen saline on blue light-induced retinal damage in rats. METHODS: The retinal damage of rats was induced by blue light exposure for 6 hours and examined 8 hours, 16 hours and 24 hours after the exposure. One hundred female Sprague-Dawley rats were randomly divided into four groups. Group 1 included 30 rats received light exposure without any other treatment. Group 2 included 30 rats received light exposure with intraperitoneal injection of normal saline. Group 3 included 30 rats received light exposure with intraperitoneal injection of saturated hydrogen saline. And Group 4 included the other 10 rats which did not receive any treatment. The amount of intraperitoneal injection of saturated hydrogen saline and normal saline was calculated in the ratio of 1ml/100g of rat weight. Specimens were collected and processed by H-E staining, ultrastructure observation, biochemical measurement. Morphological changes were observed by light microscope and transmission electron microscope (TEM) and the retinal outer nuclear layer (ONL) thickness was measured by IPP 6.0, while the malondialdehyde (MDA) was measured by colorimetric determination at 532 nm. RESULTS: Although the structure of retina in Group 1 and Group 2 was injured heavily, the injury in Group 3 was mild. The differences between Group 1 and Group 2 were not significant. Compared with the rats in Group 1 and Group 2, the ones in Group 3 had more clearly demarcated retina structure and more ordered cells by light microscope and TEM observation. The ONL thicknesses (400 times) of four groups at each time point except between Group 1 and Group 2 were significantly different (P<0.05). The thicknesses of the ONL in Group 1 at three time points were 30.41±4.04μm, 26.11±2.82μm and 20.63±1.06μm, in Group 2 were 31.62±4.54μm, 25.08±3.63μm and 19.07±3.86μm, in Group 3 were 29.75±3.62μm, 28.83±1.97μm and 27.61±1.83μm. In Group 4 the mean of the thickness was 37.35±1.37μm. As time went by, the damage grew more severely. At 24h point, the differences were most significant. Compared with Group 4, the thickness was 46.23% thinner in Group 1, 50.29% thinner in Group 2 and 28.04% thinner in Group 3. The stack structures of membranous disc in Group 3 were injured slightly, but in Group 1 and Group 2 the damage was more obvious by TEM. Compared with Group 4 at each time point, the content of MDA in Group 1 was higher (P<0.05). The content of MDA in Group 3 was significantly lower than those of Group 1 (P<0.05) and Group 2 (P<0.05). Between the Group 1 and Group 2, the MDA concentration at each time point was no significant difference (P>0.05). CONCLUSION: Saturated hydrogen saline could protect the retina from light-induced damage by attenuating oxidative stress.     

The diurnal susceptibility of rat retinal photoreceptors to light-induced damage

Exposure of albino rats to high intensity light results in rapid, graded loss of photoreceptors. The hormonal status and age of an animal at the time of exposure affect the severity of light-induced retinal damage. The adrenal axis and pituitary hormones (prolactin) have been demonstrated previously to affect the degree of cell death in the retina. Because circadian rhythms for adrenal and pituitary secretion have been demonstrated in the rat, a series of experiments was undertaken to determine if a diurnal pattern of retinal susceptibility to light damage exists which might be related to endogenous endocrine rhythms. Male Sprague-Dawley rats were exposed to 4 hr of high intensity fluorescent light for 8 consecutive days during different phases of the 14:10 hr light: dark animal room light cycle. Morphometric analysis performed at the light microscopic level 2 weeks after exposure demonstrated a differential susceptibility to light-induced cell death depending upon the period during the light-dark cycle when animals received their daily light exposure. Neuronal cell death was confined to the outer nuclear layer as previously described. The retinas of animals exposed during the middle of the dark period or during the first 5 hr of the light period were significantly more damaged than the retinas of animals exposed during the last 9 hr of the light period. Control groups for the relative amounts of dark-adaptation between groups suggested that the diurnal susceptibility to light damage was not solely dependent upon the degree of dark adaptation. These results demonstrate a diurnal susceptibility of photoreceptors to light-induced cell death.     

人脐带间充质干细胞对大鼠视网膜光损伤的保护作用

目的　观察体外人脐带间充质干细胞（human umbilical cord mesenchymal stem cells，hUCMSCs）能否由视网膜匀浆上清液诱导分化为神经样细胞及移植到视网膜光损伤大鼠玻璃体内后存活、迁移、整合及分化的情况。方法　无菌条件下采集健康足月剖宫产胎儿的正常脐带组织，经2.5 g·L^-1胰蛋白酶和1 g·L^-1胶原酶消化、贴壁培养获得hUCMSCs。将CM-Dil标记的hUCMSCs注入光损伤大鼠玻璃体内，观察眼内整合分化情况，对正常对照组、光损伤组、PBS治疗组和hUCMSCs治疗组大鼠视网膜外核层层数和厚度进行对比分析。结果　hUCMSCs培养48 h后贴壁生长，呈长梭形，14 d后可见细胞融合成片。光损伤后大鼠视网膜外核层结构紊乱、细胞层数减少，厚度变薄，与正常对照组［（40.73±1.32）μm］相比，hUCMSCs治疗组［（31.28±1.79）μm］与PBS治疗组［（17.21±1.02）μm］及光损伤组［（12.68±1.42）μm］的视网膜外核层厚度均变薄（均为P<0.05）。与光损伤组相比，PBS治疗组和hUCMSCs治疗组视网膜外核层层数显著增加。结论　HUCMSCs移植到光损伤大鼠玻璃体内后能存活、迁移及整合到受损伤视网膜，hUCMSCs玻璃体内移植可抑制光损伤大鼠光感受器的凋亡。     

The effects of the pineal gland on light-induced retinal photoreceptor damage.

Light-induced retinal photoreceptor degeneration was compared in pinealectomized and sham-pinealectomized rats at 40, 50 and 60 days of age. There was no significant difference in retinal damage between pinealectomized and sham-pinealectomized rats when they were subjected to light treatment at 40 or 50 days. However, 60-day-old pinealectomized rats showed less photoreceptor damage than did 60-day-old intact sham-pinealectomized rats when both groups were exposed to light treatment. The results suggest that the pineal gland plays a role in retinal metabolism. An hypothesis to explain the results is discussed; the effects of the pineal gland on the susceptibility of the retinal to photic damage is speculated to be endocrine in nature.