简介：目的：研究在高糖条件下,从海藻中萃取的新型多糖化合物对高糖诱导的视网膜色素上皮（RPE）细胞异常增殖的保护作用.方法：将体外培养的RPE细胞分为空白组、高糖组和多糖化合物组,空白组为正常RPE细胞培养液,高糖组为含30mmol/L葡萄糖的培养液,多糖化合物组为含30mmol/L葡萄糖和200mg/L多糖化合物的培养液.应用MTT法测量36h内不同时间点（6,12,24和36h）高糖以及多糖化合物对RPE细胞增殖影响.结果：高糖导致RPE细胞异常增殖,多糖化合物组RPE的细胞异常增殖明显得到保护,与高糖组比较差异具有统计学意义（P〈0.01）.结论：从海藻中萃取的新型多糖化合物可以明显保护高糖所导致的RPE细胞的异常增殖.

简介：目的：观察链脲佐菌素（STZ）诱发糖尿病大鼠在造模后血-视网膜屏障（blood—retinabarrier，BRB）变化情况，并以阳性药为对照研究中药芪灯明目胶囊对STZ诱发糖尿病大鼠的视网膜血管渗漏影响。方法：采用STZ腹腔注射制作糖尿病大鼠模型，在造模后6too内各时点（2wk；1，2，3，4，5，6mo）采用伊文思蓝灌注示踪显示血一视网膜的渗漏情况，在造模后3too开始用中药芪灯明目胶囊（低中高剂量组分别给予125，250，500mg／kg体质量剂量的胶囊内容物灌胃），对照组用安多明胶囊（200mg／kg体质量剂量，相当于10倍成人剂量），灌胃3mo，观察药物对BRB的影响。结果：STZ糖尿病大鼠在2wk即可出现BRB的损害，并随着高血糖状态的持续而不断加重。对造模3tooSTZ糖尿病模型大鼠连续灌胃中药芪灯治疗3mo，结果提示：中药芪灯对STZ糖尿病BRB有保护作用，可明显减少视网膜血管的渗漏。结论：STZ糖尿病模型大鼠在早期即可出现BRB损害，并随着高血糖的持续而加重，中药芪灯明目胶囊可减少高血糖导致的BRB损害。

简介：AIM:TodiscusstheimpactofLyciumBarbarumPolysaccharide(LBP)andDanshensupurifiedfromTraditionalChineseMedicine(TCM)onvascularendothelialgrowthfactor(VEGF)ofrabbitswithretinalneovascularization.METHODS:Fortyrabbitsweredividedintonormalcontrolgroup,modelcontrolgroup,LBPgroupandDanshensugroup.Animalsinthenormalcontrolgroupwerefedinthenormaloxygenenvironment.Animalsintheotherthreegroupswereputintotheenvironmentwith70%oxygenfor5daysinordertobuildthemodelofoxygen-inducedvascularproliferationretinopathy.AndthendifferentTCMextractwasinjectedintotheabdominalcavitiesoftheseannimals.After7days,theVEGFcontentofintheserumofrabbitwasmeasuredbydoubleantibodysandwichmethod.RESULTS:DataanalysisindicatedthatVEGFcontentwasasfollows:Danshensugroupwaslowerthanmodelcontrolgroup(12.92±3.84ng/Lvs19.32±4.15ng/L,P<0.05);LBPgroupandnormalcontrolgroupwerelowerthanmodelcontrolgroup(12.92±3.84ng/L,9.26±1.61ng/Lvs19.32±4.15ng/L,P<0.01);totalbloodviscosity,plasmaviscosity,cholesterolcontent,fibrinogencontentandtriacylglycerolcontentafterperitonealinjectionofLBPandDanshensuwereobviouslylowerthanbeforeinjection.CONCLUSION:TCMextract-LBPandDanshensucanprominentlyreducethecontentofVEGFintheprocessofvascularproliferativeretinopathyofrabbit;canpreventtheoccurrenceofretinalmicrovasculardiseasebyimprovingpartialoxygen-deficientenvironmentoraffectingallkindsofnewgrowthfactor.

简介：AIM:ToexploretheinhibitoryeffectofasustainedcyclosporinA(CsA)deliverymicrosphere(CsA-MS)onposteriorcapsularopacification(PCO)inrabbiteyesaftercataractextraction.·METHODS:TwentyNewZealandwhiterabbitsacceptedcataractextractionplusintraocularlensimplantationandtheirlefteyeswereintraoperativelyinjectedCsA-MSpreparedusingpolymerpolylactioglycolicacid(PLGA)asacarrierandtheirrighteyeswereinjectedwithemptyMS.Thechangesincornea,anteriorchamberreaction,intraocularpressure,PCOandCsAconcentrationinaqueoushumorwereexaminedpostoperativelyandalltheeyeswereenucleated3monthsaftersurgeryforhistopathologicalandmorphologicalexaminationwithlightmicroscopyandelectronmicroscopy.·RESULTS:Conjunctivalhyperemia,cornealedema,intraocularpressureandanteriorchamberresponseofexperimentalandcontroleyesweresimilar,whilePCOinCsAMSinjectedeyeswasgreatlyimprovedcomparedwiththatincontroleyes.PosteriorcapsulesinCsA-MSinjectedeyesweresmoothandlensepithelialcells(LEC)didnotproliferatesignificantly(P>0.05),whileLECinposteriorcapsuleofcontroleyeshaddifferentdegreesofproliferationandcorticalregeneration.LECinCsA-MSinjectedeyeswerenotfunctionallyactiveandunderwentapoptosis,whereasLECincontroleyeswerefunctionallyactive(F-test,P=0.025).Inaddition,thecornealultrastructureshowednodifferencesbetweenCsA-MSandMSinjectedeyes.CONCLUSION:CsA-MShashighbioavailabilityinrabbiteyesandcouldinhibitpostoperativePCOoccurrenceanddevelopmentduringthestudyperiod,suggestingthatCsA-MSmaybeapromising,effectiveandsafeadministrationroutetopreventPCOinclinic.