白藜芦醇对青光眼视网膜氧化损伤的保护作用

目的　探讨白藜芦醇对青光眼视网膜氧化损伤的保护作用。方法　３０只健康雄性成年家兔随机分为对照组、模型组和白藜芦醇治疗组,每组１０只。模型组和白藜芦醇治疗组用２５ｇ?Ｌ－１羟丙基甲基纤维素溶液０．２ｍＬ注入家兔前房内,制作青光眼模型。白藜芦醇治疗组按每日３００ｍｇ?ｋｇ－１体质量给予白藜芦醇灌胃,对照组和模型组给予等体积生理盐水灌胃。给药２８ｄ后测定视网膜抗氧化酶超氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ,ＳＯＤ）、谷胱甘肽过氧化物酶（ｇｌｕｔａｔｈｉｏｎｅｐｅｒｏｘｉｄａｓｅ,ＧＰＸ）和过氧化氢酶（ｃａｔａｌａｓｅ,ＣＡＴ）的活性,抗氧化物质还原型谷胱甘肽（ｇｌｕｔａｔｈｉｏｎｅ,ＧＳＨ）和还原型抗坏血酸（ａｓｃｏｒｂｉｃａｃｉｄ,ＡｓＡ）含量及一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ,ＮＯ）和丙二醛（ｍｅｔｈａｎｅｄｉｃａｒｂｏｘｙｌｉｃａｌｄｅｈｙｄｅ,ＭＤＡ）的含量。结果　模型组视网膜抗氧化酶ＳＯＤ、ＧＰＸ、ＣＡＴ活性及抗氧化物质ＧＳＨ、ＡｓＡ含量分别为（４２．０±３．３）Ｕ?ｍｇ－１、（１８．３±１．７）Ｕ?ｍｇ－１、（１．９±０．２）Ｕ?ｍｇ－１、（３３．３±２．７）ｍｇ?ｍｇ－１和（９７．０±７．６）ｍｇ?ｍｇ－１,均低于对照组（均为Ｐ＜０．０５）;ＮＯ和ＭＤＡ含量分别为（３７．０±２．９）μｍｏｌ?ｍｇ－１和（１８．０±１．７）μｍｏｌ?ｍｇ－１,均高于对照组（均为Ｐ＜０．０５）。白藜芦醇治疗组视网膜上述抗氧化酶活性、ＧＳＨ和ＡｓＡ含量分别为（４９．２±２．９）Ｕ?ｍｇ－１、（２４．１±３．２）Ｕ?ｍｇ－１、（２．８±０．２）Ｕ?ｍｇ－１、（４３．０±３．５）ｍｇ?ｍｇ－１和（１０８．４±８．１）ｍｇ?ｍｇ－１,均高于模型组,但低于对照组（均为Ｐ＜０．０５）;ＮＯ和ＭＤＡ含量分别为（３０．１±２．４）μｍｏｌ?ｍｇ－１和（１２．４±１．０）μｍｏｌ?ｍｇ－１,低于模型组,但高于对照组（均为Ｐ＜０．０５）。结论　白藜芦醇能够增加视网膜抗氧化酶活性和抗氧化物质ＧＳＨ和ＡｓＡ含量,从而可以减青光眼视网膜的氧化应激损伤。     

同型半胱氨酸和视黄醇结合蛋白4与糖尿病视网膜病变的相关性研究

目的　检测并分析同型半胱氨酸（ｈｏｍｏｃｙｓｔｅｉｎｅ,Ｈｃｙ）及视黄醇结合蛋白４（ｒｅｔｉ-ｎｏｌｂｉｎｄｉｎｇｐｒｏｔｅｉｎ４,ＲＢＰ４）与糖尿病视网膜病变（ｄｉａｂｅｔｉｃｒｅｔｉｎｏｐａｔｈｙ,ＤＲ）的关系,以探讨对特定人群ＤＲ的诊断方法。方法　选取２０１４年６月到２０１５年６月桂林医学院附属医院内分泌科就诊的２型糖尿病患者２００例,所有患者进行眼底检查必要时行眼底荧光血管造影（ｆｕｎｄｕｓｆｌｕｏｒｅｓｃｅｉｎａｎｇｉｏｇｒａｐｈｙ,ＦＦＡ）,根据眼底情况分为增殖期糖尿病视网膜病变（ｐｒｏｌｉｆｅｒａｔｉｖｅｄｉａｂｅｔｉｃｒｅｔｉｎｏｐａｔｈｙ,ＰＤＲ）组、非增殖期糖尿病视网膜病变（ｎｏｎ-ｐｒｏｌｉｆｅｒａｔｉｖｅｄｉ-ａｂｅｔｉｃｒｅｔｉｎｏｐａｔｈｙ,ＮＰＤＲ）组,以及非糖尿病视网膜病变（ｎｏｎ-ｄｉａｂｅｔｉｃｒｅｔｉｎｏｐａｔｈｙ,ＮＤＲ）组;检测各组空腹血糖（ｆａｓｔｉｎｇｐｏｓｔｐｒａｎｄｉａｌｇｌｕｃｏｓｅ,ＦＰＧ）、餐后２ｈ血糖（２-ｈｏｕｒｐｏｓｔｐｒａｎｄｉａｌｇｌｕｃｏｓｅ,２ｈＰＧ）、糖化血红蛋白（ｇｌｙｃｏｓｙｌａｔｅｄｈｅｍｏｇｌｏｂｉｎ,ＨｂＡ１ｃ）、血脂、Ｈｃｙ、ＲＢＰ４水平。结果　ＰＤＲ组的Ｈｃｙ（１７．６０±４．４７）μｍｏｌ·Ｌ－１、ＲＢＰ４（１６．３２±３．５７）μｇ·ｍＬ－１及ＮＰＤＲ组的Ｈｃｙ（１３．０１±２．８０）μｍｏｌ·Ｌ－１、ＲＢＰ４（１２．２５±２．４５）μｇ·ｍＬ－１水平明显高于ＮＤＲ组的Ｈｃｙ（６．９９±２．３３）μｍｏｌ·Ｌ－１、ＲＢＰ４（８．８９±１．９０）μｇ·ｍＬ－１,且随着ＤＲ病情的进展逐渐升高,差异均有统计学意义（均为Ｐ＜０．０５）;ＰＤＲ组病程、２ｈＰＧ、ＨｂＡ１ｃ、ＴＧ、ＬＤＬ-Ｃ、Ｈｃｙ、ＲＢＰ４水平明显高于ＮＰＤＲ组、ＮＤＲ组（均为Ｐ＜０．０５）。相关分析显示,２型糖尿病患者的ＲＢＰ４与病程、年龄、ＨｂＡ１ｃ、ＦＰＧ、２ｈＰＧ、ＴＣ、ＴＧ、ＬＤＬ-Ｃ、Ｈｃｙ呈显著正相关,与ＨＤＬ-Ｃ呈负相关。对ＤＲ的危险因素进行多元回归分析结果显示,病程、ＨｂＡ１ｃ、ＲＢＰ４、Ｈｃｙ是影响ＤＲ的主要危险因素。结论　测定Ｈｃｙ及ＲＢＰ４可及早发现ＤＲ,为早期筛查及治疗提供一定的方向。     

SnoN蛋白及TGF-β在早期糖尿病大鼠视网膜组织中表达及意义

目的　观察ＳｎｏＮ蛋白及ＴＧＦ-β在糖尿病大鼠视网膜上的表达,探讨ＳｎｏＮ蛋白及ＴＧＦ-β与糖尿病视网膜病变（ｄｉａ-ｂｅｔｉｃｒｅｔｉｎｏｐａｔｈｙ,ＤＲ）的关系,为ＤＲ发病机制的研究提供新的理论依据。方法　选择健康雄性Ｗｉｓｔａｒ大鼠２０只,随机分为正常对照组与糖尿病（ＤＭ）组,每组各１０只。采用一次性腹腔注射５０ｍｇ?ｋｇ－１链脲佐菌素（ｓｔｒｅｐｔｏｚｏｔｏｃｉｎ,ＳＴＺ）的方法建立ＤＭ大鼠模型,正常对照组一次性给予等体积柠檬酸三钠-柠檬酸缓冲液腹腔注射。分别于造模后８周和１２周处死各组大鼠,均完整摘除各组大鼠的左眼球制成眼杯,采用免疫组织化学方法检测各组大鼠视网膜上ＳｎｏＮ蛋白及ＴＧＦ-β蛋白的表达。结果　造模后８周和１２周,ＤＭ组大鼠血糖值分别为（２２．６４±３．５７）ｍｍｏｌ?Ｌ－１、（２４．０８±１．６０）ｍｍｏｌ?Ｌ－１,均明显高于正常对照组的（４．６４±０．９１）ｍｍｏｌ?Ｌ－１、（４．５０±０．６６）ｍｍｏｌ?Ｌ－１,差异均有显著统计学意义（均为Ｐ＜０．０１）。正常对照组大鼠视网膜上ＴＧＦ-β无表达或弱表达,在造模后８周和１２周时,ＤＭ组大鼠视网膜上ＴＧＦ-β的ＯＤ值分别为０．１２１０±０．００５６、０．１５５０±０．００７０,均较正常对照组（０．０２２０±０．００７９、０．０２５０±０．００７０）明显增加（均为Ｐ＜０．０１）。正常对照组大鼠视网膜上ＳｎｏＮ蛋白高表达,在造模后８周和１２周时,ＤＭ组大鼠视网膜上ＳｎｏＮ的ＯＤ值分别为０．４１２０±０．０１１３、０．２１４０±０．００６９,均较正常对照组（０．９４５０±０．００７０、０．９４４０±０．００５１）明显降低（均为Ｐ＜０．０１）,且随着病程的延长,降低更明显。结论　ＳｎｏＮ蛋白对ＴＧＦ-β信号通路起负反馈抑制作用,能降低ＴＧＦ-β信号的强度和持续时间,因此对ＤＲ的防治具有重要意义。     

补精益视片对大鼠慢性高眼压模型视网膜损害的影响

目的　观察补精益视片对大鼠慢性高眼压（ｅｌｅｖａｔｅｄｉｎｔｒａｏｃｕｌａｒｐｒｅｓｓｕｒｅ,ＥＩＯＰ）模型视网膜损害的干预作用,探讨其作用机理。方法　将３０只ＳＤ大鼠随机分为３组:对照组、给药组、模型组,每组１０只。采用烙闭上巩膜静脉法对给药组、模型组ＳＤ大鼠建立慢性ＥＩＯＰ模型,观察补精益视片对慢性ＥＩＯＰ大鼠眼压和视网膜病理形态学变化的影响。结果　给药组、模型组大鼠在造模后即刻直至造模后８周与造模前相比眼压均升高,差异均有统计学意义（均为Ｐ＜０．０１）,说明ＥＩＯＰ模型造模成功。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）,模型组差异无统计学意义（Ｐ＞０．０５）。造模后８周,视网膜神经节细胞（ｒｅｔｉｎａｌｇａｎｇｌｉｏｎｃｅｌｌｓ,ＲＧＣｓ）数量给药组（１４．５７±１．９７）与模型组（１０．７６±２．１９）均明显低于对照组（１７．４７±１．９７）,差异均有统计学意义（Ｐ＜０．０５,Ｐ＜０．０１）;视网膜厚度模型组为（１５０．８３±１７．９１）μｍ低于对照组的（２１９．７２±３２．２４）μｍ,差异有统计学意义（Ｐ＜０．０１）,给药组为（２１５．５１±５１．２３）μｍ,与对照组相比差异无统计学意义（Ｐ＞０．０５）;给药组ＲＧＣｓ数量及视网膜厚度均优于模型组,差异均有统计学意义（均为Ｐ＜０．０１）。ＲＧＣｓ超微结构显示给药组较模型组明显改善。结论　补精益视片能保护ＳＤ大鼠慢性ＥＩＯＰ模型视功能,表现为降低眼压、提高ＲＧＣｓ数量、增加视网膜厚度、改善ＲＧＣｓ超微结构。     

补肾活血中药对大鼠慢性高眼压模型视网膜神经节细胞PI3K/Akt信号转导通路p-Akt表达的影响

目的　观察补肾活血中药对大鼠慢性高眼压（ｅｌｅｖａｔｅｄｉｎｔｒａｏｃｕｌａｒｐｒｅｓｓｕｒｅ,ＥＩＯＰ）模型视网膜神经节细胞（ｒｅｔｉｎａｌｇａｎｇｌｉｏｎｃｅｌｌｓ,ＲＧＣ）ＰＩ３Ｋ／Ａｋｔ信号转导通路ｐ-Ａｋｔ表达的影响。方法　３０只ＳＤ大鼠随机分成３组:对照组、模型组和给药组,模型组和给药组建立ＥＩＯＰ模型。给药组造模后每天予复方丹参片和杞菊地黄丸的混悬液灌胃,每天１次,连续８周,对照组、模型组每天予生理盐水灌胃。记录造模前、造模后即刻、造模后８周的眼压;光镜下观察各组视网膜厚度和ＲＧＣ数量,电镜下观察视网膜超微结构,免疫组织化学法检测视网膜内ｐ-Ａｋｔ的表达。结果　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）。造模后８周,给药组与模型组ＲＧＣ数量均低于对照组,差异均有统计学意义（均为Ｐ＜０．０５）;对照组视网膜厚度与给药组相比,差异无统计学意义（Ｐ＞０．０５）,而对照组与模型组相比,差异有统计学意义（Ｐ＜０．０１）;给药组ＲＧＣ数量及视网膜厚度均高于模型组,差异均有统计学意义（均为Ｐ＜０．０１）。电镜下ＲＧＣ超微结构显示,模型组损伤明显,给药组较模型组有所改善。视网膜ｐ-Ａｋｔ表达免疫组织化学结果分析显示,给药组ｐ-Ａｋｔ阳性染色总面积、平均光密度、积分光密度值与模型组相比,差异均有统计学意义（均为Ｐ＜０．０１）,给药组黑度（１３９．９７±１１．７９）虽高于模型组（１３７．９５±６．１３）,但差异无统计学意义（Ｐ＞０．０５）。结论　补肾活血中药用于ＳＤ大鼠慢性ＥＩＯＰ模型,能降低眼压,提高ＲＧＣ数量及改善超微结构,增加视网膜厚度,上调ＰＩ３Ｋ／Ａｋｔ信号转导通路中ｐ-Ａｋｔ的表达。     

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。     

正常大鼠视网膜脂质过氧化和抗氧化能力与年龄的相关研究

目的了解视网膜脂质过氧化（ｌｉｐｉｄｐｅｒｏｘｉｄａｔｉｏｎ，ＬＰＯ）和抗氧化能力与年龄的关系。方法雄性Ｗｉｓｔａｒ大鼠２２只，按５、１２、１８、２４个月龄分为４组，采用硫代巴比妥酸比色法与化学发光法检测不同月龄大鼠视网膜ＬＰＯ产物丙二醛（ｍａｌｏｎｄｉａｌｄｅｈｙｄｅ，ＭＤＡ）含量和相当于超氧化物岐化酶（ｓｕ－ｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ，ＳＯＤ）活性的抗氧化能力。结果大鼠视网膜ＭＤＡ含量：５、１２、１８、２４月龄时分别为０．１８±０．０６、０．１６±０．０６、０．３８±０．１１、０．４９±０．０９ｎｍｏｌ／ｍｇ蛋白（Ｆ检验，Ｐ＜０．０１）；大鼠视网膜ＳＯＤ活性：５、１２、１８、２４月龄时分别为０．９９±０．３０、２．４８±０．５６、０．７０±０．３５、０．８５±０．５７Ｕ／ｍｇ蛋白（ＷＴＢＸ〗Ｆ检验，Ｐ＜０．０１）。结论大鼠视网膜ＭＤＡ含量和相当于ＳＯＤ活性的抗氧化能力随年龄增加分别呈升高或下降的趋势，提示老龄视网膜ＬＰＯ增强可能是抗氧化能力下降与长期慢性光化学损伤累积作用的共同结果。     

表皮生长因子受体抑制剂抑制大胶质细胞活化对急性高眼压大鼠视网膜神经节细胞丢失的研究

目的　探讨表皮生长因子受体（ｅｐｉｄｅｒｍａｌｇｒｏｗｔｈｆａｃｔｏｒｒｅｃｅｐｔｏｒ,ＥＧＦＲ）抑制剂抑制大胶质细胞活化对实验性急性高眼压大鼠视网膜神经节细胞（ｒｅｔｉｎａｌｇａｎｇｌｉｏｎｃｅｌｌｓ, ＲＧＣｓ）丢失的影响。方法　用健康成年ＳＤ大鼠１８只,随机分为３组:空白对照组,不做任何处理;实验组采用前房灌注法制造急性高眼压模型,造模成功后,按６ｍｇ?ｋｇ－１?ｄ－１用量给予大鼠口服ＥＧＦＲ抑制剂ＡＧ１４７８;实验对照组造模成功后给予大鼠口服等量生理盐水。３组均于７ｄ处死大鼠,观察各组视网膜结构的变化及采用免疫组织化学法观察阳性节细胞的表达。结果　通过免疫组化法发现,随着造模时间的延长,视网膜结构变得模糊不清,ＲＧＣｓ阳性染色细胞逐渐减少。空白对照组、实验组、实验对照组ＲＧＣｓＴｈｙ-１阳性表达光密度值分别是:１４３．６６６７±４．０４１５、１３９．０３２２±１．７３４０和１０１．１０２３±２．０００１。实验组和空白对照组相比,视网膜Ｔｈｙ-１阳性表达差异无统计学意义（Ｐ＞０．０５）,实验对照组和空白对照组比较,差异有统计学意义（Ｐ＜０．０５）,实验组与实验对照组视网膜Ｔｈｙ-１阳性表达,差异亦有统计学意义（Ｐ＜０．０５）。结论　ＥＧＦＲ抑制剂通过抑制大胶质细胞的活化对实验性急性高眼压大鼠模型的ＲＧＣｓ有保护作用。     

高度近视眼人工晶状体度数计算公式的准确性比较

目的　评价用ＩＯＬＭａｓｔｅｒ和ＳＲＫ-Ⅱ、ＳＲＫ-Ｔ、Ｈｏｌｌａｄａｙ-１和Ｈａｉｇｉｓ四种公式计算眼轴≥２７ｍｍ的高度近视眼人工晶状体（ｉｎｔｒａｏｃｕｌａｒｌｅｎｓ,ＩＯＬ）度数的准确性。方法　回顾性分析于我院行白内障超声乳化摘出联合ＩＯＬ植入术、眼轴≥２７ｍｍ的高度近视合并白内障患者１０５例（１４８眼）的临床资料,用ＩＯＬＭａｓｔｅｒ测量并用以上四种公式计算ＩＯＬ度数和预测术后屈光度。按照眼轴长度分组,从２７ｍｍ起每增加１ｍｍ为一组,分别计算各组术后３个月时实际术后等效球镜度（ａｃｔｕａｌｐｏｓｔｏｐｅｒａｔｉｖｅｓｐｈｅｒｉｃａｌｅｑｕｉｖａｌｅｎｃｅ,ＡＰＳＥ）与四种公式计算的预测术后等效球镜度（ｐｒｅｄｉｃｔｅｄｐｏｓｔｏｐｅｒａｔｉｖｅｓｐｈｅｒｉｃａｌｅｑｕｉｖａｌｅｎｃｅ,ＰＰＳＥ）的差值,即为预测屈光度误差值（ｐｒｅｄｉｃｔｉｖｅｅｒｒｏｒ,ＰＥ）。比较四种公式在不同眼轴长度区间ＰＥ的统计学差异,将眼轴组间ＰＥ没有统计学差异的组合并得到眼轴长区间,并计算出这四种ＩＯＬ计算公式在不同眼轴长度区间的ＰＥ。结果　１４８眼眼轴长度为（３１．０６±２．３２）ｍｍ,ＰＥ在ＳＲＫ-Ⅱ、ＳＲＫ-Ｔ、Ｈｏｌｌａｄａｙ-１和Ｈａｉｇｉｓ公式分别为（１．０１±１．５３）Ｄ、（０．７６±０．９６）Ｄ、（１．２４±０．８０）Ｄ和（０．７８±０．８４）Ｄ;四种公式计算的ＰＰＳＥ与ＡＰＳＥ间差异均有统计学意义（均为Ｐ＜０．０５）,ＳＲＫ-Ｔ和Ｈａｉｇｉｓ公式的ＰＥ差异无统计学意义（Ｐ＞０．０５）;Ｈｏｌｌａｄａｙ-１公式的ＰＥ与ＳＲＫ-Ｔ、Ｈａｉｇｉｓ公式的ＰＥ均有显著差异（均为Ｐ＜０．０５）。将眼轴组间ＰＥ没有统计学差异的组合并后得到２７～３０ｍｍ、３０～３２ｍｍ、３２～３４ｍｍ、≥３４ｍｍ四个眼轴长度区间,ＳＲＫ-Ｔ／Ｈａｉｇｉｓ公式在各区间的ＰＥ分别为（０．２１±０．６５）Ｄ／（０．４８±０．７１）Ｄ、（０．５８±０．５６）Ｄ／（０．５８±０．６１）Ｄ、（１．１８±０．６７）Ｄ／（０．９７±０．６１）Ｄ和（１．９７±１．４４）Ｄ／（１．７６±１．２６）Ｄ。结论　在眼轴≥２７ｍｍ的高度近视眼ＩＯＬ度数计算上ＳＲＫ-Ⅱ、ＳＲＫ-Ｔ、Ｈａｉｇｉｓ和Ｈｏｌｌａｄａｙ-１公式预测术后屈光度均为近视方向的过矫正。在不同眼轴长度区间用ＳＲＫ-Ｔ／Ｈａｉｇｉｓ公式计算时,适当向近视方向调整ＰＰＳＥ（－０．２～－２．０）／（－０．５～－１．８）Ｄ而得到的植入ＩＯＬ度数可以改善计算公式的准确性。     

合并近视的原发性开角型青光眼眼血流动力学研究

目的：利用彩色多普勒血流显像研究合并近视的原发性开角型青光眼（Ｐｒｉｍａｒｙ Ｏｐｅｎａｎｇｌｅ Ｇｌａｕｃｏｍａｗｉｔｈ Ｍｙｏｐｉａ,ＭＰＯＡＧ）眼部血流动力学变化。方法：对３８ 例６３ 只合并近视（平均－６．９２ ±３ ．７９Ｄ）高眼压性（ 平均眼压３２ ．００±９．３６ｍｍＨｇ）ＰＯＡＧ、３２ 例５１ 只单纯原发性开角型青光眼（Ｓｉｍｐｌｅ Ｐｒｉｍａｒｙ Ｏｐｅｎａｎｇｌｅ Ｇｌａｕｃｏｍａ,ＳＰＯＡＧ） 、１５ 例３０ 只正常眼分别测量眼动脉、视网膜中央动脉、睫状后动脉的收缩期血流峰值速度（ＰＳＶ） 、舒张末期血流速度（ＥＤＶ） 、阻力指数（ＲＩ） 。结果：①与正常组比较：ＭＰＯＡＧ组及ＳＰＯＡＧ组视网膜中央动脉及睫状后动脉的ＲＩ升高（ Ｐ＜０．０５,Ｐ＜０ ．０１） ;ＭＰＯＡＧ 组眼动脉的ＥＤＶ值减低（Ｐ＜０．０５） 。②与ＳＰＯＡＧ 组比较：ＭＰＯＡＧ组眼动脉ＥＤＶ值明显减低（Ｐ＜ ０．０１）。结论：ＭＰＯＡＧ 患者眼部血流速度减低,血管阻力升高,有血流灌注不足的表现。提示眼压及血管因素在高眼压性ＭＰＯＡＧ 的视功能损害中均起着重要作用。     

葛花总黄酮对糖尿病小鼠视网膜MDA、SOD的影响

目的探讨葛花总黄酮（TFF）对糖尿病小鼠视网膜抗氧化损伤的作用。方法加只C57BL／6J小鼠随机分为5组：正常对照组、糖尿病（DM）模型组、TFF小剂量组（TFFⅠ）、中剂量组（TFFⅡ）和大剂量组（TFFⅢ）。DM、TFFⅠ、TFFⅡ和TFFⅢ组造模成功后第5周开始给药,给药10周,于第15周测定小鼠血糖和体重,处死小鼠取眼球,测定各组小鼠视网膜过氧化终产物丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性。结果与模型组（血糖120．98±5．57mmol／L,体重21．55±1．67g）比较,给予TFF中剂量组血糖（13．51±6．09mmol／L）和大剂量组血糖（9．66±2．86mmol／L）显著下降（P〈0．01）,大剂量组（体重24．50±1．58g）可明显改善体重的下降（P〈0．01）。与模型组（MDA含量：12．10±1．06nmol／mgprot,SOD活性：8．45±0．95U／mgprot）相比,TFF小、中、大剂量组MDA含量均明显降低（MDA含量分别为：7．98±0．40、5．75±0．63、5．24±0．48nmol／mgprot,P〈0．01）,SOD活性均明显升高（SOD活性分别为：13．10±0．90、17．28±0．94、17．79±1．21U／mgprot,P〈0．01）。结论TFF能增强糖尿病小鼠视网膜抗氧化能力,减轻视网膜的氧化损伤,从而对糖尿病视网膜病变起一定保护作用。     

The effect of L-carnitine in the prevention of ionizing radiation-induced cataracts: a rat model

Background The objective was to determine the antioxidant role of L-carnitine (LC) against ionizing radiation-induced cataracts in lens after total cranium irradiation of rats with a single dose of 5 Gy. Methods Sprague-Dawley rats were used in this experiment and were divided into three groups. Group 1 did not receive LC or irradiation (control group). Group 2 received a 5 Gy gamma irradiation as a single dose to the total cranium (RT group). Group 3 received total cranium irradiation plus 100 mg/kg body weight/day LC (RT+LC group). The rats were irradiated using a cobalt-60 teletherapy unit. At the end of the 10th day, the rats were sacrificed and their eyes were enucleated. The lenticular activity of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured. Furthermore, the lenticular content of an indicator of lipid peroxidation, malondialdehyde (MDA), was measured. Results Irradiation significantly increased the MDA level as an end product of lipid peroxidation. Irradiation also significantly decreased SOD activity and increased GSH-Px activity, indicating the generation of oxidative stress and an early protective response to oxidative damage. Irradiation with 5 Gy to the total cranium as a single fraction formed cataracts in the rat lenses. Cataract development was detectable in 9 rats in the RT group, and in only 4 rats in the RT+LC group 10 days after irradiation. LC administration plus irradiation significantly decreased the MDA level and increased the activity of SOD and GSH-Px enzymes, which might indicate the protection of the lenses from gamma radiation-induced cataracts. Conclusions L-carnitine may protect against the damage produced by gamma radiation by increasing the activity of the SOD enzyme and by scavenging free radicals generated by ionizing radiation. As a result of this process, MDA as an indicator of lipid peroxidation may decrease.     

放射性视网膜病变大鼠玻璃体与血清血管内皮生长因子的相关研究

目的通过放射性^60Co照射SD大鼠制作放射性视网膜病变（RR）模型,探讨在RR的发展中,血管内皮生长因子（VEGF）的作用。方法45只SD大鼠,随机分为正常对照组、10Gy组和30Gy组,每组15只。^60Co射线照射制作RR模型。分别于3、6、9个月时检测RR大鼠血清及玻璃体中的VEGF质量浓度,并制作大鼠视网膜毛细血管铺片。结果30Gy组与10Gy组大鼠玻璃体中VEGF浓度较正常对照组增高,差异均有统计学意义（P〈0.01）。30Gy组与10Gy组大鼠血清中VEGF质量浓度与正常对照组比较差异均无统计学意义（P〉0.05）。实验组大鼠视网膜毛细血管铺片结果显示,随时间延长视网膜微血管病变逐渐加重。结论在RR大鼠模型中,VEGF参与RR的发展。随时间延长玻璃体中VEGF质量浓度增加,后者与RR视网膜微血管病变的发展呈正相关,为临床上治疗RR提供理论依据。     

Effects of Oral <Emphasis Type="Italic">Ginkgo biloba</Emphasis> Supplementation on Cataract Formation and Oxidative Stress Occurring in Lenses of Rats Exposed to Total Cranium Radiotherapy

Purpose To determine the antioxidant role of Ginkgo biloba (GB) in preventing radiation-induced cataracts in the lens after total-cranium irradiation of rats with a single radiation dose of 5Gy.Methods Sprague-Dawley rats were randomly divided into three groups. Group 1 received neither GB nor irradiation (control group). Group 2 was exposed to total-cranium irradiation of 5Gy in a single dose [radiation therapy (RT) Group], and group 3 received total cranium irradiation from a cobalt-60 teletherapy unit, plus 40mg/kg per day GB (RT+GB group). At the end of the tenth day, the rats were killed and their eyes were enucleated to measure the antioxidant enzymes, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the lipid peroxidation level [malondialdehyde (MDA)].Results Irradiation significantly increased both the MDA level and the activity of GSH-Px, and significantly decreased the activity of SOD in the rat lenses. GB supplementation significantly increased the activities of SOD and GSH-Px enzymes and significantly decreased the MDA level. Total cranium irradiation of 5Gy in a single dose promoted cataract formation, and GB supplementation protected the lenses from radiation-induced cataracts.Conclusions We suggest that Ginkgo biloba is an antioxidant that protects the rat lens from radiation-induced cataracts. Jpn J Ophthalmol 2004;48:499–502 © Japanese Ophthalmological Society 2004     

Protective role of intramuscularly administered vitamin E on the levels of lipid peroxidation and the activities of antioxidant enzymes in the lens of rats made cataractous with gamma-irradiation

PURPOSE: To determine the antioxidant role of vitamin E (VE) (10 mg/kg/day) against radiation-induced cataract in lens after total-cranium irradiation of rats with a single dose of 5 Gy. METHODS: Sprague-Dawley rats were divided into three groups. Group 1 did not receive VE or irradiation but received both 0.1 ml physiologic saline intraperitoneally and sham irradiation (control group). Group 2 received to total cranium 5 Gy of gamma irradiation as a single dose (RT group) plus 0.1 ml physiologic saline intraperitoneally. Group 3 received irradiation to total cranium plus 10 mg/kg/day VE (RT+VE group). The rats were irradiated using a cobalt-60 teletherapy unit. Chylack's cataract classification (1) was used in this study. At the end of 10 days, the rats were killed and their eyes were enucleated to measure the antioxidant enzymes (the activity of superoxide dismutase [SOD], glutathione peroxidase [GSH-Px]) and lipid peroxidation level (malondialdehyde [MDA]). RESULTS: While grade 1 cataract development was detectable in seven rats in the RT group, it was detectable only in two rats in the RT+VE group, whereas none of the rats in the control group exhibited any biomicroscopic change in their lenses. MDA level and GSH-Px activity in the rat lens in the RT group was significantly higher than in the control group. SOD activity in the RT group was lower than in the control group. The activity of SOD and GSH-Px enzymes was higher in the RT+VE group, but MDA level was lower in the RT+VE group when compared with the RT group. CONCLUSIONS: Vitamin E has a protective effect on radiation-induced cataract by decreasing oxidative stress.     

The age-related macular degeneration radiotherapy trial (AMDRT): one year results from a pilot study

PURPOSE: To assess the short-term safety and efficacy of treating subfoveal choroidal neovascularization (CNV) with external beam radiation delivered in 5 x 4 Gy fractions among patients having age-related macular degeneration (AMD). DESIGN: A multicenter prospective randomized controlled pilot study. METHODS: Eighty-eight patients were enrolled through 10 sites and were randomized to radiotherapy (20 Gy delivered in 5 daily fractions of 4 Gy each; 6 MV [N = 41]) or no radiotherapy (sham radiotherapy [N = 22] or observation [N = 25]). Eligibility criteria included visual acuity of at least 20/320 and subfoveal CNV not amenable to treatment. Randomization was stratified by lesion type (new or recurrent CNV) and blood (<50% or >/=50% of the lesion [N = 13]). The primary outcome measure was loss of >/=3 lines of visual acuity. Secondary outcome measures were angiographic response and side effects. RESULTS: At baseline, patient and ocular characteristics were similar between treatment groups. At six months, 9 radiated eyes (26%) and 17 eyes not radiated (49%) lost >/=3 lines of visual acuity (P = .04; stratified chi(2) test). At 12 months, 13 radiated eyes (42%) and 9 observed eyes (49%) lost >/=3 visual acuity lines (P = .60). The radiated group demonstrated smaller lesions and less fibrosis than the nonradiated group (P = .05 and .004, respectively) at 12 months. Radiation-induced complications were not observed except for one radiated eye with numerous cotton wool spots and possible radiation retinopathy. CONCLUSIONS: External beam radiation at 5 x 4 Gy may have a modest and short-lived (six month) benefit in preserving visual acuity.     

紫外线对培养兔晶体的氧化损伤及超微形态学研究

目的 探讨实验性兔晶体氧自由基损伤与白内障的发病机制。方法 利用近距离紫外线（ＵＶ）照射体外培养兔晶体,诱发氧自由基损伤。并同时观察超氧化物歧化酶（ＳＯＤ）的抗氧化作用。实验分为ＵＶ照射组、ＵＶ＋ＳＯＤ组及对照组,采用硫代巴比妥酸比色法分别检测三组晶体匀浆中脂质过氧化产物丙二醛含量,并通过透射电镜观察三组晶体上皮细胞的超微结构。结果 ＵＶ照射组兔晶体匀浆中的丙二醛含量明显增高。ＵＶ＋ＳＯＤ组（ＵＶ     

葡萄籽原花青素调控NLRP3/Caspase-1通路介导的焦亡途径对糖尿病视网膜病变大鼠的保护作用

目的　探讨葡萄籽原花青素调控NLRP3/Caspase-1通路介导的焦亡途径对糖尿病视网膜病变（DR）大鼠的保护作用。方法　建立DR大鼠模型，随机分为模型组、葡萄籽原花青素组、VX-765组、葡萄籽原花青素+VX-765组（每组各12只），另取12只大鼠为对照组，药物干预14 d，HE染色观察各组大鼠视网膜组织病理学变化；TUNEL染色检测各组大鼠视网膜神经节细胞（RGC）焦亡情况；采用试剂盒测定各组大鼠视网膜组织超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、活性氧（ROS）、丙二醛（MDA）及血清中炎症因子糖基化终末产物（AGEs）、白细胞介素（IL）-1β与IL-18水平；Western blot检测各组大鼠视网膜组织NLRP3/Caspase-1通路蛋白表达水平。结果　与对照组相比，模型组大鼠视网膜组织明显变薄，结构疏松，细胞结构层次紊乱、排列不规则，RGC变少、稀疏，呈现严重病理损伤变化，RGC焦亡率，ROS与MDA水平，AGEs、IL-1β、IL-18水平，NLRP3与Caspase-1蛋白表达水平均显著升高（均为P<0.05），SOD与CAT水平均显著降低（均为P<0.05）。与模型组相比，葡萄籽原花青素组、VX-765组大鼠视网膜组织形态结构得到恢复，病理损伤均有不同程度减轻，RGC焦亡率，ROS与MDA水平，AGEs、IL-1β与IL-18水平，NLRP3与Caspase-1蛋白表达水平均降低（均为P<0.05），SOD与CAT水平均升高（均为P<0.05）。与葡萄籽原花青素组及VX-765组分别相比，葡萄籽原花青素+VX-765组大鼠视网膜组织病理损伤进一步减轻，形态结构几乎恢复正常，RGC焦亡率，ROS与MDA水平，AGEs、IL-1β与IL-18水平，NLRP3与Caspase-1蛋白表达水平均降低（均为P<0.05），SOD与CAT水平均升高（均为P<0.05）。结论　葡萄籽原花青素可以抑制炎症发生发展，增强DR大鼠抗氧化活性，减轻过氧化反应，缓解视网膜组织病理学损伤，减少RGC焦亡，可能是通过抑制NLRP3/Caspase-1信号通路实现的。