祛障穴冷冻疗法与随机改变冷冻位点对亚硒酸钠诱导大鼠白内障抑制作用差异性的实验研究
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摘要
目的:
1.建立大鼠白内障模型,并探讨亚硒酸钠诱导大鼠白内障模型晶状体混浊的发生机制。
2.探讨祛障穴冷冻疗法和改变冷冻位点对亚硒酸钠诱导大鼠白内障模型晶状体混浊进展的抑制和延缓机制。
3.通过对祛障穴冷冻疗法和改变冷冻位点方式的对比分析,探索优势冷冻位点,并探讨后者针对年龄相关性白内障治疗的有效性和可行性。
4.为低温生物医学揭示冷冻对白内障抑制延缓作用的机理提供宝贵资料。
方法:
对35只大鼠行裂隙灯检查,排除晶状体病变。随机抽取5只大鼠作为正常对照组,其余大鼠随机分为3组,每组10只,隔日于颈背部皮下注射1mmol/ L的亚硒酸钠,共注射3次,正常组给予等剂量0.9%生理盐水,监测大鼠晶状体混浊变化。待晶状体刚刚出现混浊时,祛障穴冷冻治疗组大鼠给予祛障穴冷冻疗法,每周1次,5周一疗程,方法参照李永才发明祛障穴冷冻疗法。冷冻位点改变治疗组大鼠,于大鼠角巩膜缘12点位每次随机抽取4位点,行冷冻治疗,操作方法同祛障穴冷冻治疗组。未治疗组不予处理。通过裂隙灯观察并记录大鼠晶状体混浊的进展。晶状体混浊分级标准采用英国牛津大学眼科实验室方法。6wk时处死大鼠,取出晶状体,测定其中水溶性蛋白质含量、谷胱甘肽(GSH)含量、谷胱甘肽还原酶(GR)及过氧化氢酶(CAT)活性。
结果:
1.除正常组以外,其余三组大鼠双眼均于1wk开始出现混浊,2wk～6wk白内障未治疗组大鼠双眼晶状体混浊进展较快,而两治疗组大鼠双眼晶状体相对B组混浊进展较慢,且混浊程度轻于B组,具有高度统计学意义(右:P=0.000,左:P=0.002)。
2.晶状体可溶性蛋白质含量,与正常组相比,未治疗组大鼠显著降低,有高度统计学意义(右:P=0.010,左:P=0.001),祛障穴冷冻组右眼、冷冻位点改变组双眼低于正常组,但无统计学意义(P>0.05),祛障穴冷冻组左眼眼较正常组显著降低,具有高度统计学意义(P=0.016)。
3.GR活性,各组大鼠双眼晶状体比较其差别无统计学意义(P>0.05);
4.GSH比较,与正常组大鼠双眼比较白内障未治疗组、祛障穴冷冻组和冷冻位点改变治疗组双眼晶状体GSH含量明显降低,有高度统计学意义(P=0.000,P=0.000,P=0.000)。
5.CAT活性,与正常组大鼠双眼比较白内障未治疗组、祛障穴冷冻组和冷冻位点改变治疗组双眼晶状体CAT活性明显降低,有高度统计学意义(P=0.000,P=0.000,P=0.000)。祛障穴冷冻组和冷冻位点改变治疗组CAT活性高于白内障未治疗组,右眼分别为41.4%和35.9%(P=0.003,P=0.012),左眼分别为32.3%和27.4%(P=0.008,P=0.031),具有高度统计学意义。
6.色素沉着,祛障穴冷冻组和冷冻位点改变治疗组在对大鼠角巩膜缘进行冷冻治疗瞬间均形成冻斑,随即冻斑消失,6wk少数祛障穴冷冻组大鼠角巩膜缘冷冻位点处出现不同程度色素沉着,而这一表现在冷冻位点改变治疗组大鼠中未能出现。
结论:
1.亚硒酸钠诱导大鼠白内障模型是白内障发病机制及疗效评价的可靠模型。
2.晶状体内氧化损伤可能贯穿于白内障的发生发展。
3.祛障穴冷冻疗法对大鼠初发期白内障晶状体混浊有较好的抑制、延缓作用
4.祛障穴冷冻疗法与随机改变4冷冻位点在对白内障大鼠晶状体混浊的抑制、延缓作用的比较中无显著性差异,而后者能够更好的分散由冷冻对局部组织引起的刺激和伤害。
5.依据祛障穴冷冻疗法治疗老年性未成熟期白内障规范化整理研究成果(国家中医药管理局诊疗技术课题,国中医药科2001ZL27号),预计角巩膜缘随机选取4冷冻位点冷冻治疗年龄相关性白内障将取得较好疗效。
Purpose:
1. Cataract model in rats, and sodium selenite cataract model induced by the mechanism of lens opacity.
2. To explore Qu Zhang Point cryosurgery and changing the freezing point sites on the selenite cataract model induced by inhibition of the progress of lens opacity and delay mechanisms.
3. By Qu Zhang Point cryosurgery and changing the freezing point cryotherapy sites the way comparative analysis of the latter effect for the treatment of senile cataract the predictability and feasibility.
Methods:
35 rats were slit lamp examination to exclude the lens disease. 5 rats were randomly selected as normal control group, the remaining rats were randomly divided into 3 groups of 10 each, every other day subcutaneous injection in the neck, 1mmol / L of sodium selenite were injected three times the normal group was given 0.9% saline, monitoring changes in lens opacity. Lens opacity appears to be just when the treatment group of Qu Zhang Point cryosurgery to cured by Qu Zhang Point cryosurgery, 1 time a week, 5 Mon treatments, methods, invented by Mr Li You cai’Qu Zhang Point cryosurgery. Freezing changes the treatment sites of the rats in the rat limbal 12 randomly selected 4-bit each time point to cryosurgery, use the same methods as Qu Zhang Point cryosurgery group. Through the slit lamp to observe and record the progress of rat lens opacification. Lens opacity classification criterion used by the laboratory method of Ophthalmology, University of Oxford. 6wk rats were sacrificed, remove the lens to determine which water-soluble protein, glutathione (GSH), glutathione reductase (GR) and catalase (CAT) activity.
Results:
1. In addition to the normal group than the other three rats eyes were cloudy began in 1wk, 2wk～6wk untreated cataract lens opacity group eyes rapid progress, while the two treatment group eyes the progress of lens opacities compared with the relative B group slow, and the turbidity and light in the B group, the difference was significant (right:P=0.000,.left:P=0.002).
2. Lens soluble protein content, compared with the normal group, no treatment group were significantly lower, with statistical significance (right: P = 0.010, left: P = 0.001), Qu Zhang Point cryosurgery right eye point freezing group, frozen sites change the group with normal control eyes, but no statistical significance (P>0.05), the left eye of Qu Zhang Point cryosurgery group were significantly lower than normal (P = 0.016).
3.GR activity, each rat eye lens compare the difference was not statistically significant (P>0.05);
4.GSH comparison, compared with normal rats of cataract eyes without treatment, Qu Zhang Point cryosurgery group and removing of point freezing treatment group,eyes sites to change the lens GSH concentration decreased and there was significant difference (P = 0.000, P = 0.000, P = 0.000).
5.CAT activity, compared with normal rats of cataract eyes without treatment, Qu Zhang Point cryosurgery group and removing of point freezing treatment group sites change CAT activity was significantly lower lens eyes, there was significant difference (P = 0.000, P = 0.000, P = 0.000). Qu Zhang Point cryosurgery group and removing of point freezing treatment group sites change CAT activity in the treatment group than in untreated patients with cataract, right eye were 41.4% and 35.9% (P = 0.003, P = 0.012), left eye were 32.3% and 27.4% ( P = 0.008, P = 0.031), with statistical significance.
6. Pigmentation, Qu Zhang Point cryosurgery group and removing of point freezing treatment group change in position on the rats in the treatment group were frozen treat limbal formation of cold spots are an instant, then cold spots disappeared, 6wk few Qu Zhang Point cryosurgery group limbal frozen rats frozen sites pigmentation appears at different levels, and this reflected in the frozen site failed to change the treatment group there.
Conclusion:
1. Selenite cataract model induced cataract pathogenesis and treatment evaluation of reliableModel.
2. The lens oxidative damage may run through the development of cataracts.
3. Qu Zhang Point cryosurgery group onset of cataract in rat lens opacity has good inhibition, delay Slow effect.
4. Qu Zhang Point cryosurgery group and removing of point freezing of randomly selecting for each 4 sites treatment group Limbal rats were in dialogue, impaired inhibition of rat lens opacity and delay comparison of the role of no significant difference, while the later can be better distributed by the freezing of the local tissue irritation and damage caused.
5. According to dispel the Qu Zhang Point cryosurgery treatment of senile cataract is not mature research results standardized order (State Administration of Traditional treatment technology issues, the National Bureau 2001ZL27 number of Chinese medicine), is expected to limbal frozen each 4 sites were randomly selected treatment age-related cataract will get better effect.
1.建立大鼠白内障模型,并探讨亚硒酸钠诱导大鼠白内障模型晶状体混浊的发生机制。
2.探讨祛障穴冷冻疗法和改变冷冻位点对亚硒酸钠诱导大鼠白内障模型晶状体混浊进展的抑制和延缓机制。
3.通过对祛障穴冷冻疗法和改变冷冻位点方式的对比分析,探索优势冷冻位点,并探讨后者针对年龄相关性白内障治疗的有效性和可行性。
4.为低温生物医学揭示冷冻对白内障抑制延缓作用的机理提供宝贵资料。
方法:
对35只大鼠行裂隙灯检查,排除晶状体病变。随机抽取5只大鼠作为正常对照组,其余大鼠随机分为3组,每组10只,隔日于颈背部皮下注射1mmol/ L的亚硒酸钠,共注射3次,正常组给予等剂量0.9%生理盐水,监测大鼠晶状体混浊变化。待晶状体刚刚出现混浊时,祛障穴冷冻治疗组大鼠给予祛障穴冷冻疗法,每周1次,5周一疗程,方法参照李永才发明祛障穴冷冻疗法。冷冻位点改变治疗组大鼠,于大鼠角巩膜缘12点位每次随机抽取4位点,行冷冻治疗,操作方法同祛障穴冷冻治疗组。未治疗组不予处理。通过裂隙灯观察并记录大鼠晶状体混浊的进展。晶状体混浊分级标准采用英国牛津大学眼科实验室方法。6wk时处死大鼠,取出晶状体,测定其中水溶性蛋白质含量、谷胱甘肽(GSH)含量、谷胱甘肽还原酶(GR)及过氧化氢酶(CAT)活性。
结果:
1.除正常组以外,其余三组大鼠双眼均于1wk开始出现混浊,2wk～6wk白内障未治疗组大鼠双眼晶状体混浊进展较快,而两治疗组大鼠双眼晶状体相对B组混浊进展较慢,且混浊程度轻于B组,具有高度统计学意义(右:P=0.000,左:P=0.002)。
2.晶状体可溶性蛋白质含量,与正常组相比,未治疗组大鼠显著降低,有高度统计学意义(右:P=0.010,左:P=0.001),祛障穴冷冻组右眼、冷冻位点改变组双眼低于正常组,但无统计学意义(P>0.05),祛障穴冷冻组左眼眼较正常组显著降低,具有高度统计学意义(P=0.016)。
3.GR活性,各组大鼠双眼晶状体比较其差别无统计学意义(P>0.05);
4.GSH比较,与正常组大鼠双眼比较白内障未治疗组、祛障穴冷冻组和冷冻位点改变治疗组双眼晶状体GSH含量明显降低,有高度统计学意义(P=0.000,P=0.000,P=0.000)。
5.CAT活性,与正常组大鼠双眼比较白内障未治疗组、祛障穴冷冻组和冷冻位点改变治疗组双眼晶状体CAT活性明显降低,有高度统计学意义(P=0.000,P=0.000,P=0.000)。祛障穴冷冻组和冷冻位点改变治疗组CAT活性高于白内障未治疗组,右眼分别为41.4%和35.9%(P=0.003,P=0.012),左眼分别为32.3%和27.4%(P=0.008,P=0.031),具有高度统计学意义。
6.色素沉着,祛障穴冷冻组和冷冻位点改变治疗组在对大鼠角巩膜缘进行冷冻治疗瞬间均形成冻斑,随即冻斑消失,6wk少数祛障穴冷冻组大鼠角巩膜缘冷冻位点处出现不同程度色素沉着,而这一表现在冷冻位点改变治疗组大鼠中未能出现。
结论:
1.亚硒酸钠诱导大鼠白内障模型是白内障发病机制及疗效评价的可靠模型。
2.晶状体内氧化损伤可能贯穿于白内障的发生发展。
3.祛障穴冷冻疗法对大鼠初发期白内障晶状体混浊有较好的抑制、延缓作用
4.祛障穴冷冻疗法与随机改变4冷冻位点在对白内障大鼠晶状体混浊的抑制、延缓作用的比较中无显著性差异,而后者能够更好的分散由冷冻对局部组织引起的刺激和伤害。
5.依据祛障穴冷冻疗法治疗老年性未成熟期白内障规范化整理研究成果(国家中医药管理局诊疗技术课题,国中医药科2001ZL27号),预计角巩膜缘随机选取4冷冻位点冷冻治疗年龄相关性白内障将取得较好疗效。
Purpose:
1. Cataract model in rats, and sodium selenite cataract model induced by the mechanism of lens opacity.
2. To explore Qu Zhang Point cryosurgery and changing the freezing point sites on the selenite cataract model induced by inhibition of the progress of lens opacity and delay mechanisms.
3. By Qu Zhang Point cryosurgery and changing the freezing point cryotherapy sites the way comparative analysis of the latter effect for the treatment of senile cataract the predictability and feasibility.
Methods:
35 rats were slit lamp examination to exclude the lens disease. 5 rats were randomly selected as normal control group, the remaining rats were randomly divided into 3 groups of 10 each, every other day subcutaneous injection in the neck, 1mmol / L of sodium selenite were injected three times the normal group was given 0.9% saline, monitoring changes in lens opacity. Lens opacity appears to be just when the treatment group of Qu Zhang Point cryosurgery to cured by Qu Zhang Point cryosurgery, 1 time a week, 5 Mon treatments, methods, invented by Mr Li You cai’Qu Zhang Point cryosurgery. Freezing changes the treatment sites of the rats in the rat limbal 12 randomly selected 4-bit each time point to cryosurgery, use the same methods as Qu Zhang Point cryosurgery group. Through the slit lamp to observe and record the progress of rat lens opacification. Lens opacity classification criterion used by the laboratory method of Ophthalmology, University of Oxford. 6wk rats were sacrificed, remove the lens to determine which water-soluble protein, glutathione (GSH), glutathione reductase (GR) and catalase (CAT) activity.
Results:
1. In addition to the normal group than the other three rats eyes were cloudy began in 1wk, 2wk～6wk untreated cataract lens opacity group eyes rapid progress, while the two treatment group eyes the progress of lens opacities compared with the relative B group slow, and the turbidity and light in the B group, the difference was significant (right:P=0.000,.left:P=0.002).
2. Lens soluble protein content, compared with the normal group, no treatment group were significantly lower, with statistical significance (right: P = 0.010, left: P = 0.001), Qu Zhang Point cryosurgery right eye point freezing group, frozen sites change the group with normal control eyes, but no statistical significance (P>0.05), the left eye of Qu Zhang Point cryosurgery group were significantly lower than normal (P = 0.016).
3.GR activity, each rat eye lens compare the difference was not statistically significant (P>0.05);
4.GSH comparison, compared with normal rats of cataract eyes without treatment, Qu Zhang Point cryosurgery group and removing of point freezing treatment group,eyes sites to change the lens GSH concentration decreased and there was significant difference (P = 0.000, P = 0.000, P = 0.000).
5.CAT activity, compared with normal rats of cataract eyes without treatment, Qu Zhang Point cryosurgery group and removing of point freezing treatment group sites change CAT activity was significantly lower lens eyes, there was significant difference (P = 0.000, P = 0.000, P = 0.000). Qu Zhang Point cryosurgery group and removing of point freezing treatment group sites change CAT activity in the treatment group than in untreated patients with cataract, right eye were 41.4% and 35.9% (P = 0.003, P = 0.012), left eye were 32.3% and 27.4% ( P = 0.008, P = 0.031), with statistical significance.
6. Pigmentation, Qu Zhang Point cryosurgery group and removing of point freezing treatment group change in position on the rats in the treatment group were frozen treat limbal formation of cold spots are an instant, then cold spots disappeared, 6wk few Qu Zhang Point cryosurgery group limbal frozen rats frozen sites pigmentation appears at different levels, and this reflected in the frozen site failed to change the treatment group there.
Conclusion:
1. Selenite cataract model induced cataract pathogenesis and treatment evaluation of reliableModel.
2. The lens oxidative damage may run through the development of cataracts.
3. Qu Zhang Point cryosurgery group onset of cataract in rat lens opacity has good inhibition, delay Slow effect.
4. Qu Zhang Point cryosurgery group and removing of point freezing of randomly selecting for each 4 sites treatment group Limbal rats were in dialogue, impaired inhibition of rat lens opacity and delay comparison of the role of no significant difference, while the later can be better distributed by the freezing of the local tissue irritation and damage caused.
5. According to dispel the Qu Zhang Point cryosurgery treatment of senile cataract is not mature research results standardized order (State Administration of Traditional treatment technology issues, the National Bureau 2001ZL27 number of Chinese medicine), is expected to limbal frozen each 4 sites were randomly selected treatment age-related cataract will get better effect.
引文
[1] AsbellPA, DualanI, MindelJ,etal.Age-relatedcataract[J].Lancet, 2005,365(9459):599-609
[2] Hockwin O teal.Dev Ophthalmol.2002,35:1
[3] Nordmann J.Adv Ophthalmol,1962,12:1
[4] Nordmann J.Adv Ophthalmol,1977,34:1
[5] Hiller R etal.Am J Epidemiol,1986,124:916
[6] Spector A etal.Exp Eye Res,1981,33:67
[7] Shinohara T etal.J Ocul Pharmacol Ther,2000,16:181
[8]刘学东.硒性白内障研究现状[J].微量元素与健康研究,2000,17 (1):68-70.
[9]诸葛国民,李耐三.白内障防治药物研究进展.中国药科大学学报.1992,23(6):382.
[10]宋念艺,刘连生.补锌对白内障大鼠晶状体NO和NOS的影响[J].湖北省卫生职工医学院学报,2004,17(3):8-10.
[11] ORHAN H,MAROL S,HEPSEN I F,et al.Effects of some probable antioxidants on selenite-induced cataract formation and Oxidative stress-related parameters in rats[J].Toxicology,1999,139(3):219-232.
[12]范莉琼,曹阳,岑洁等.硒性白内障模型与人老年性白内障比较研究[J].眼科新进展,2005,25(3):248-250
[13]郑宏,于普林,洪依舒,等.我国城乡老年人白内障的患病情况调查[J]中华流行病学杂志,2001,22 (6) :446-448
[14] TruscottR J1Age-rel atednuc learc atara ct-oxid ationis thekey [J].ExpEyeRes,2005,80(5):709-725
[15] WilliamsSL, FerrignoL, MoraP, etal.Baselinec ataracttype And 10 Year mortality in the Italian-Americancasecontrolstudyofagerelated cataract [J]. American journal of epidemiology,2002,156(2):127-131
[16] BigsbyRM,CardenasH,GrantAC,etal.Protective effects of estrogeninara- tmodel ofage-related cataracts[J].Proc Nat Acad Sci USA,1999,96 (16):9328-9332
[17] YounanC,MitchelP,CummingRG,etal.Hormone replacement therapy, reproduc- tive factors,and the incidence of cataract and cataract surgery[J]. American Journal of Epidemiology,2002,155:11
[18] AinaFO,SmeethL,HubbardR,etal.Hormonerepla cement therapy and cataract: apopulation-basedcase-controlstudy[J].Eye,2005,22
[19] KleinBE,KleinR,LeeKE1.Reproductive exposures,incidentage related cataracts, andage-related maculopathyinwomen: the BeaverDam Eye Study [J].AmJ Ophthalmol,2000,130:322-326
[20] HammondCJ,SniederH,SpectotrTD,etal.Geneticand environmental FActor sina- gerelated nuclear cataract inmonozygotic and dizygotic twins[J]. NEnglJMed,2000,342:1786-1790
[21] HammondCJ,DuncanDD,LangeMD,etal.Genesand environment incortical cataract: the twin eye study[J]. Invest Ophthal molVis Sci,2000,41:2901
[22] 14CongdonN,BrowanKW,LaiH,etal.Nuclear cataract shows signifycant familia laggregation in an old erpopulation after adjusttment for possible share dencironmental factors [J].Investigation ophthalmology & visualscience, 2004,45(7):2182-2186
[23] WestSK,DuncanDD,MunozB,etal.Sun light exposure and risk of lens Opacitie- sina population-basedstudy:the SalisburyEy-eEvaluation Project[J]. JAMA,1998,280:714-718
[24] DolinPJ.Ultravioletradiation and cataract:are view of the epidemicological evidence[J].BrJOphthalmol,1994,78:478-482
[25] HuFB,HankinsonSE,StampferMJ,etal.Prospective study of ca taract extraction and risk of coronaryheart disease[J]. Amercian Journal of Epidemiology, 2001,153:875-881
[26] ZigmanS,McDanielT,SchultzJB,etal.Damage to culture dlensepi the Lialcellsofsquirrelsandrabbits by UV-A ( 99.9% ) plus UV-B(0.1%) radiation and alphatocopherol protection[J].MolCellBiochem, 1995,143:35-46
[27] ZigmanS.UltravioletAandCataracts:Basic Research and Practical Applications [J].Internationa lO phthalmology,2005,45(1):29-40
[28] CongdonNG.Prevention strategies for agerelated cataract: present limita- tions and future possibilities[J].Br J Ophthalmol,2001,85:516-520
[29]李自成,曹茂银,宋翠娥,等.高血压病患者血清载脂蛋白与视网膜动脉硬化的关系[J].湖北医科大学学报,1996,17(4):340-342
[30]张其英,蒋宝林.高血压高血脂高血糖与老年性白内障的关系[J] .淮海医药,1999,17(3):37
[31]MeyerD,MaritzFJ,LiebenbergPH,etal.Corticallensopacities In the young patient an indication foralipogram South African medical journal[J]. 2001,91(6):520-524
[32]HillerR,SperdutoRD,ReedGF.Serumlipidsandage-related-Lensopac-ities:along it udinalinve stigation:the Framingham Studies [J].Oph-thalmology, 2003,110(3):578-583
[33]Inoue1KJ,Kubota1SC,TsuruT,etal.Cholestanol InducesAp-optosis- Of CornealEndothelialandLens Epithelial Cells[J].Investigative Ophthal- mology and Visual Science,2000,41:991-997
[34] DelamereN .As corbicacid and the eye[J].SubcellBiochem, 1996,25:313-329
[35] ChristenWG 1Antioxidantvitaminsandage-relatedeyedise- ase [J]. Proc- AssAmPhys, 1999,111:16-21
[36]ChristenWG,GlynnRJ,AjaniUA,etal .Smokingcessation and risk of agerela- tedcataractinmen[J].JAMA,2000,284:713-716
[37]Yan H, Harding JJ, Hui YN, et al. The decreased chaperone activi-ty ofα-crystallin in selenite cataractmay result from seleniteinduced- aggregation[J]. Eye, 2003, 17(5) : 637 - 645.
[38]周建,惠延年,李燕,等.波形纤维蛋白在其转基因小鼠晶状体的表达[J].眼科学报, 1999, 15:199-203
[39] Lingner J, Hughes TR, Shevchenko A,etal.Reverse tran- scrip tasemotify in the catalytic subunit of telomerase. Science 1997;276: 561-567
[40] MeyersonM. Role of telomerase in normal and cancer cells. [J] Clin Oncol200;18:2626-2634
[41] Mason DX, Goneska E, Greider CW. Stem-loop N of te- trahymena telomerase RNA stimulates p rocessivity in trans. Mol Cell B iol 2003;23(16):5606-5613
[42] Colitz CM, DavidsonMG, McgahanMC. Telomerase activity in lens epithelial cells of normal and cataractous lenses. Exp Eye Res 1999;69:641-649
[43] McElligott R, Wellinger RJ. The terminalDNA structure Of Mammalianchromo- somes. EMBO J 1997;16:3705-3714
[44]徐国兴,武莉莉,郑学栋,等.年龄相关性白内障晶状体上皮细胞凋亡与端粒酶的表达.中国临床康复2005;9(18):158-159
[45] Colitz CMH, Malarkey D, DykstraMJ, etal. Histologic and immunohistochemical characterization of lens cap sule p lagues in dogs with cata-racts. Am J Vet Res 2000;61(2):139-143
[46] Cao Y, Li H, Mu FT, etal. Telomerase activation causes vascular smooth muscle cell p roliferation in genetic hypertension. FAS EB 2002;16(1):96-98
[47]刘燕,周健,刘新平,等. MRG15的克隆及其在正常和年龄相关性白内障晶状体上皮细胞中的表达.眼科研究2005;23(3):228-231
[48] Ashe PC, BerryMD. Apop totic signaling cascades. Prog N euro Psychopharm acol B iol Psychiarty 2003;27(2):199-214
[49]李青,杨佩菲.凋亡相关基因Caspase29在年龄相关性白内障晶状体上皮细胞中的表达及意义.福建医药杂志2006;28(2):1-2
[50]钱益勇,李侲宇,张振平,等.鞘脂酶激活蛋白在年龄相关性白内障晶状体上皮细胞的表达.眼视光学杂志2007;9(3):149-151
[51] Malina H, Richter C, Frueh B, etal. Lens ep ithelial cell apop tosisand intracellular Ca2+ increase in the p resence of xanthurenic acid. BMCOphthalm ol 2002;2(1):1-7
[52] WirtzMK, Xu H, Rust K. Insulin-like growth factor bind- ing p rotein-5 exp ression by human trabecular mesh work. Invest Ophthalm ol V is Sci1998;39(1):45-53
[53]华夏,孙慧敏,苑晓勇,等. IGFBP25和Lamp-2在年龄相关性白内障和透明晶状体上皮细胞的蛋白表达.国际眼科杂志2006,6(6) :1287-1290
[54]范伟,吉祥,喻长泰,等.晶状体上皮细胞凋亡及bcl-2、bax表达与年龄相关性白内障形成的关系.眼视光学杂志2003,5(2):75-78
[55]江文珊,阴正勤.成年及幼年Long-evans大鼠视皮层HSP8基因的表达差异.国际眼科杂志2008,8(1):29-31
[56] Derham BK, Harding JJ. Effects of modifications of alpha crystallinon its chaperone and other p roperties. B iochem J 2002;364 (Pt3):711-717
[57] Bu L, J in Y, Shi Y, etal. Mutant DNA2binding domain of HSF 4 isassociated with autosomal dominant lamellar andMarner cataract. N atureGenet 2002;31(3):276
[58] Casado A, de la Torre R, Lopez2Fernandez E. Antioxidant Enzymelevels in red blood cells from cataract patients. Gerontology 2001;47(4):186-188
[59] Lee EH, Joo CK. Role of transform ing growth factor-βin transdiffer- entiation and fibrosis of lens ep ithelial cells. Invest Ophthalm ol V is Sci1999;40(9):2025-2032
[60]徐雯,姚克,王凯军,吴仁毅,孙朝辉.钙蛋白酶抑制剂PD1 50606对鼠氧化性白内障的预防作用[J].中华眼科杂志2003,39:400-405.
[61] PikeBR , ZhaoX ,Newcomb J K. Stretchinjury causes cal-painand caspase-3 activation and necroticand apoptotic cell death insept ohippocampal cell cultures [J].J Ne u-rotrauma 2000,17:283-298.
[62] Wolf BB ,Schuler M , Eche verri F. Cspase 3 is the pr imary activator of apoptotic DNA fragmentation via DNA fragmentation factor-45/ inhibitor of caspase activate d D naseinactivation [J].J Boil Chem 1999;274 :30651 -30656.
[63] Singh D P , Ohoguro N. Lensepithelium derived growth factor: effects on growth and survival of lensepithelial cells , keratinocytes and fibroblasts [J] . Biochem Bi ophys Res Commmun 2000;267 :373-381.
[64] Fatma N ,Singh D P , Shinohara T. Transcriptional reg ulation of the antioxidant protein2ge ne , athiol-specif ic antioxidant ,by lensepithe lium-derived growth fac tor top rotect cells from oxidative stress [ J ] . J Bi ol Chem 2001;276 :48899-48907.
[65]马尚龄.浙江中医学院学报, 1995, 19 (5): 22
[66]邬凤岩,林华英.福建中医院, 1995, 26 (2): 12
[67]孟慧,王传富,孙禄来.山东中医杂志, 1995, 14(1): 13-14
[68]刘立安,王福隆,孙剑文.针刺治疗老年性白内障的临床观察[J].中医眼科杂志, 1992,2(3):149
[69]李新民.耳穴结扎治疗白内障未成熟期150例[J].上海针灸杂志1992,11(2):27
[70]侍广全.消障灵治疗早期老年性白内障疗效观察[J].中国中医眼科杂志,1993,3 (1):8-11
[71]赵长涛.中药熏灸治疗未成熟期白内障34例[J].中医外治杂志,2000,9(6):23
[72]李菊琦.隔核桃壳灸并耳压法治老年性白内障疗效总结[J].江西中医药,1991,22(5):37
[73]魏丽娟,夏青艳.祛障穴冷冻疗法治疗老年性进行期白内障机理研究. [J].江西中医药,1994,25:47
[74]董万国,聂天祥.祛障穴冷冻治疗老年性白内障临床观察[J].中西医结合眼科杂志,1995,13(3):173
[75]李树星,李籽祯,李真.口服障明星片配合眼穴冷冻治疗早期老年性白内障[J].中西医结合眼科杂志,1998,16(3):13-15
[76]郝振海,刘冬玲,刘宁.亚硒酸钠诱发大鼠白内障实验方法的改进[J].眼科新进展,1993,13(3):12
[77] Ajiboye R,Hdaring JJ. The non-nezymic glycosylation of bovine lens proteins by glucosamine and its inhibition by aspirin,ibuprofen and glutathione [J].ExP Eye Res,1989;49(l):31～41.
[2] Hockwin O teal.Dev Ophthalmol.2002,35:1
[3] Nordmann J.Adv Ophthalmol,1962,12:1
[4] Nordmann J.Adv Ophthalmol,1977,34:1
[5] Hiller R etal.Am J Epidemiol,1986,124:916
[6] Spector A etal.Exp Eye Res,1981,33:67
[7] Shinohara T etal.J Ocul Pharmacol Ther,2000,16:181
[8]刘学东.硒性白内障研究现状[J].微量元素与健康研究,2000,17 (1):68-70.
[9]诸葛国民,李耐三.白内障防治药物研究进展.中国药科大学学报.1992,23(6):382.
[10]宋念艺,刘连生.补锌对白内障大鼠晶状体NO和NOS的影响[J].湖北省卫生职工医学院学报,2004,17(3):8-10.
[11] ORHAN H,MAROL S,HEPSEN I F,et al.Effects of some probable antioxidants on selenite-induced cataract formation and Oxidative stress-related parameters in rats[J].Toxicology,1999,139(3):219-232.
[12]范莉琼,曹阳,岑洁等.硒性白内障模型与人老年性白内障比较研究[J].眼科新进展,2005,25(3):248-250
[13]郑宏,于普林,洪依舒,等.我国城乡老年人白内障的患病情况调查[J]中华流行病学杂志,2001,22 (6) :446-448
[14] TruscottR J1Age-rel atednuc learc atara ct-oxid ationis thekey [J].ExpEyeRes,2005,80(5):709-725
[15] WilliamsSL, FerrignoL, MoraP, etal.Baselinec ataracttype And 10 Year mortality in the Italian-Americancasecontrolstudyofagerelated cataract [J]. American journal of epidemiology,2002,156(2):127-131
[16] BigsbyRM,CardenasH,GrantAC,etal.Protective effects of estrogeninara- tmodel ofage-related cataracts[J].Proc Nat Acad Sci USA,1999,96 (16):9328-9332
[17] YounanC,MitchelP,CummingRG,etal.Hormone replacement therapy, reproduc- tive factors,and the incidence of cataract and cataract surgery[J]. American Journal of Epidemiology,2002,155:11
[18] AinaFO,SmeethL,HubbardR,etal.Hormonerepla cement therapy and cataract: apopulation-basedcase-controlstudy[J].Eye,2005,22
[19] KleinBE,KleinR,LeeKE1.Reproductive exposures,incidentage related cataracts, andage-related maculopathyinwomen: the BeaverDam Eye Study [J].AmJ Ophthalmol,2000,130:322-326
[20] HammondCJ,SniederH,SpectotrTD,etal.Geneticand environmental FActor sina- gerelated nuclear cataract inmonozygotic and dizygotic twins[J]. NEnglJMed,2000,342:1786-1790
[21] HammondCJ,DuncanDD,LangeMD,etal.Genesand environment incortical cataract: the twin eye study[J]. Invest Ophthal molVis Sci,2000,41:2901
[22] 14CongdonN,BrowanKW,LaiH,etal.Nuclear cataract shows signifycant familia laggregation in an old erpopulation after adjusttment for possible share dencironmental factors [J].Investigation ophthalmology & visualscience, 2004,45(7):2182-2186
[23] WestSK,DuncanDD,MunozB,etal.Sun light exposure and risk of lens Opacitie- sina population-basedstudy:the SalisburyEy-eEvaluation Project[J]. JAMA,1998,280:714-718
[24] DolinPJ.Ultravioletradiation and cataract:are view of the epidemicological evidence[J].BrJOphthalmol,1994,78:478-482
[25] HuFB,HankinsonSE,StampferMJ,etal.Prospective study of ca taract extraction and risk of coronaryheart disease[J]. Amercian Journal of Epidemiology, 2001,153:875-881
[26] ZigmanS,McDanielT,SchultzJB,etal.Damage to culture dlensepi the Lialcellsofsquirrelsandrabbits by UV-A ( 99.9% ) plus UV-B(0.1%) radiation and alphatocopherol protection[J].MolCellBiochem, 1995,143:35-46
[27] ZigmanS.UltravioletAandCataracts:Basic Research and Practical Applications [J].Internationa lO phthalmology,2005,45(1):29-40
[28] CongdonNG.Prevention strategies for agerelated cataract: present limita- tions and future possibilities[J].Br J Ophthalmol,2001,85:516-520
[29]李自成,曹茂银,宋翠娥,等.高血压病患者血清载脂蛋白与视网膜动脉硬化的关系[J].湖北医科大学学报,1996,17(4):340-342
[30]张其英,蒋宝林.高血压高血脂高血糖与老年性白内障的关系[J] .淮海医药,1999,17(3):37
[31]MeyerD,MaritzFJ,LiebenbergPH,etal.Corticallensopacities In the young patient an indication foralipogram South African medical journal[J]. 2001,91(6):520-524
[32]HillerR,SperdutoRD,ReedGF.Serumlipidsandage-related-Lensopac-ities:along it udinalinve stigation:the Framingham Studies [J].Oph-thalmology, 2003,110(3):578-583
[33]Inoue1KJ,Kubota1SC,TsuruT,etal.Cholestanol InducesAp-optosis- Of CornealEndothelialandLens Epithelial Cells[J].Investigative Ophthal- mology and Visual Science,2000,41:991-997
[34] DelamereN .As corbicacid and the eye[J].SubcellBiochem, 1996,25:313-329
[35] ChristenWG 1Antioxidantvitaminsandage-relatedeyedise- ase [J]. Proc- AssAmPhys, 1999,111:16-21
[36]ChristenWG,GlynnRJ,AjaniUA,etal .Smokingcessation and risk of agerela- tedcataractinmen[J].JAMA,2000,284:713-716
[37]Yan H, Harding JJ, Hui YN, et al. The decreased chaperone activi-ty ofα-crystallin in selenite cataractmay result from seleniteinduced- aggregation[J]. Eye, 2003, 17(5) : 637 - 645.
[38]周建,惠延年,李燕,等.波形纤维蛋白在其转基因小鼠晶状体的表达[J].眼科学报, 1999, 15:199-203
[39] Lingner J, Hughes TR, Shevchenko A,etal.Reverse tran- scrip tasemotify in the catalytic subunit of telomerase. Science 1997;276: 561-567
[40] MeyersonM. Role of telomerase in normal and cancer cells. [J] Clin Oncol200;18:2626-2634
[41] Mason DX, Goneska E, Greider CW. Stem-loop N of te- trahymena telomerase RNA stimulates p rocessivity in trans. Mol Cell B iol 2003;23(16):5606-5613
[42] Colitz CM, DavidsonMG, McgahanMC. Telomerase activity in lens epithelial cells of normal and cataractous lenses. Exp Eye Res 1999;69:641-649
[43] McElligott R, Wellinger RJ. The terminalDNA structure Of Mammalianchromo- somes. EMBO J 1997;16:3705-3714
[44]徐国兴,武莉莉,郑学栋,等.年龄相关性白内障晶状体上皮细胞凋亡与端粒酶的表达.中国临床康复2005;9(18):158-159
[45] Colitz CMH, Malarkey D, DykstraMJ, etal. Histologic and immunohistochemical characterization of lens cap sule p lagues in dogs with cata-racts. Am J Vet Res 2000;61(2):139-143
[46] Cao Y, Li H, Mu FT, etal. Telomerase activation causes vascular smooth muscle cell p roliferation in genetic hypertension. FAS EB 2002;16(1):96-98
[47]刘燕,周健,刘新平,等. MRG15的克隆及其在正常和年龄相关性白内障晶状体上皮细胞中的表达.眼科研究2005;23(3):228-231
[48] Ashe PC, BerryMD. Apop totic signaling cascades. Prog N euro Psychopharm acol B iol Psychiarty 2003;27(2):199-214
[49]李青,杨佩菲.凋亡相关基因Caspase29在年龄相关性白内障晶状体上皮细胞中的表达及意义.福建医药杂志2006;28(2):1-2
[50]钱益勇,李侲宇,张振平,等.鞘脂酶激活蛋白在年龄相关性白内障晶状体上皮细胞的表达.眼视光学杂志2007;9(3):149-151
[51] Malina H, Richter C, Frueh B, etal. Lens ep ithelial cell apop tosisand intracellular Ca2+ increase in the p resence of xanthurenic acid. BMCOphthalm ol 2002;2(1):1-7
[52] WirtzMK, Xu H, Rust K. Insulin-like growth factor bind- ing p rotein-5 exp ression by human trabecular mesh work. Invest Ophthalm ol V is Sci1998;39(1):45-53
[53]华夏,孙慧敏,苑晓勇,等. IGFBP25和Lamp-2在年龄相关性白内障和透明晶状体上皮细胞的蛋白表达.国际眼科杂志2006,6(6) :1287-1290
[54]范伟,吉祥,喻长泰,等.晶状体上皮细胞凋亡及bcl-2、bax表达与年龄相关性白内障形成的关系.眼视光学杂志2003,5(2):75-78
[55]江文珊,阴正勤.成年及幼年Long-evans大鼠视皮层HSP8基因的表达差异.国际眼科杂志2008,8(1):29-31
[56] Derham BK, Harding JJ. Effects of modifications of alpha crystallinon its chaperone and other p roperties. B iochem J 2002;364 (Pt3):711-717
[57] Bu L, J in Y, Shi Y, etal. Mutant DNA2binding domain of HSF 4 isassociated with autosomal dominant lamellar andMarner cataract. N atureGenet 2002;31(3):276
[58] Casado A, de la Torre R, Lopez2Fernandez E. Antioxidant Enzymelevels in red blood cells from cataract patients. Gerontology 2001;47(4):186-188
[59] Lee EH, Joo CK. Role of transform ing growth factor-βin transdiffer- entiation and fibrosis of lens ep ithelial cells. Invest Ophthalm ol V is Sci1999;40(9):2025-2032
[60]徐雯,姚克,王凯军,吴仁毅,孙朝辉.钙蛋白酶抑制剂PD1 50606对鼠氧化性白内障的预防作用[J].中华眼科杂志2003,39:400-405.
[61] PikeBR , ZhaoX ,Newcomb J K. Stretchinjury causes cal-painand caspase-3 activation and necroticand apoptotic cell death insept ohippocampal cell cultures [J].J Ne u-rotrauma 2000,17:283-298.
[62] Wolf BB ,Schuler M , Eche verri F. Cspase 3 is the pr imary activator of apoptotic DNA fragmentation via DNA fragmentation factor-45/ inhibitor of caspase activate d D naseinactivation [J].J Boil Chem 1999;274 :30651 -30656.
[63] Singh D P , Ohoguro N. Lensepithelium derived growth factor: effects on growth and survival of lensepithelial cells , keratinocytes and fibroblasts [J] . Biochem Bi ophys Res Commmun 2000;267 :373-381.
[64] Fatma N ,Singh D P , Shinohara T. Transcriptional reg ulation of the antioxidant protein2ge ne , athiol-specif ic antioxidant ,by lensepithe lium-derived growth fac tor top rotect cells from oxidative stress [ J ] . J Bi ol Chem 2001;276 :48899-48907.
[65]马尚龄.浙江中医学院学报, 1995, 19 (5): 22
[66]邬凤岩,林华英.福建中医院, 1995, 26 (2): 12
[67]孟慧,王传富,孙禄来.山东中医杂志, 1995, 14(1): 13-14
[68]刘立安,王福隆,孙剑文.针刺治疗老年性白内障的临床观察[J].中医眼科杂志, 1992,2(3):149
[69]李新民.耳穴结扎治疗白内障未成熟期150例[J].上海针灸杂志1992,11(2):27
[70]侍广全.消障灵治疗早期老年性白内障疗效观察[J].中国中医眼科杂志,1993,3 (1):8-11
[71]赵长涛.中药熏灸治疗未成熟期白内障34例[J].中医外治杂志,2000,9(6):23
[72]李菊琦.隔核桃壳灸并耳压法治老年性白内障疗效总结[J].江西中医药,1991,22(5):37
[73]魏丽娟,夏青艳.祛障穴冷冻疗法治疗老年性进行期白内障机理研究. [J].江西中医药,1994,25:47
[74]董万国,聂天祥.祛障穴冷冻治疗老年性白内障临床观察[J].中西医结合眼科杂志,1995,13(3):173
[75]李树星,李籽祯,李真.口服障明星片配合眼穴冷冻治疗早期老年性白内障[J].中西医结合眼科杂志,1998,16(3):13-15
[76]郝振海,刘冬玲,刘宁.亚硒酸钠诱发大鼠白内障实验方法的改进[J].眼科新进展,1993,13(3):12
[77] Ajiboye R,Hdaring JJ. The non-nezymic glycosylation of bovine lens proteins by glucosamine and its inhibition by aspirin,ibuprofen and glutathione [J].ExP Eye Res,1989;49(l):31～41.