简介:目的:探讨褪黑素对过氧化氢诱导晶状体上皮细胞氧化损伤的保护作用。方法:晶状体上皮细胞传代培养后,分别加入不同浓度褪黑素预处理12h后,加入100μmol/LH2O2继续孵育24h,MTT比色法检测褪黑素对H2O2诱导的晶状体上皮细胞活力的影响,流式细胞仪检测细胞凋亡率,比色法检测凋亡相关因子Caspase-3及Caspase-9的活性。结果:MTT结果显示褪黑素对晶状体上皮细胞活性无影响,该药物可以抑制过氧化氢诱导的细胞活性的下降,流式细胞计数结果显示褪黑素可以抑制过氧化氢诱导的细胞凋亡,此外,褪黑素还可以减少过氧化氢所致晶状体上皮细胞内Caspase-3及Caspase-9的活性,并且,伴随褪黑素作用时间的延长其活性呈下降趋势。结论:褪黑素可以明显抑制过氧化氢诱导的晶状体上皮细胞的凋亡,从而为寻求有效的防治白内障药物提供可靠的实验依据。
简介:AIM:Toexploretheeffectofsaturatedhydrogensalineonbluelight-inducedretinaldamageinrats.·METHODS:Theretinaldamageofratswasinducedbybluelightexposurefor6hoursandexamined8hours,16hoursand24hoursaftertheexposure.OnehundredfemaleSprague-Dawleyratswererandomlydividedintofourgroups.Group1included30ratsreceivedlightexposurewithoutanyothertreatment.Group2included30ratsreceivedlightexposurewithintraperitonealinjectionofnormalsaline.Group3included30ratsreceivedlightexposurewithintraperitonealinjectionofsaturatedhydrogensaline.AndGroup4includedtheother10ratswhichdidnotreceiveanytreatment.Theamountofintraperitonealinjectionofsaturatedhydrogensalineandnormalsalinewascalculatedintheratioof1ml/100gofratweight.SpecimenswerecollectedandprocessedbyH-Estaining,ultrastructureobservation,biochemicalmeasurement.Morphologicalchangeswereobservedbylightmicroscopeandtransmissionelectronmicroscope(TEM)andtheretinalouternuclearlayer(ONL)thicknesswasmeasuredbyIPP6.0,whilethemalondialdehyde(MDA)wasmeasuredbycolorimetricdeterminationat532nm.·RESULTS:AlthoughthestructureofretinainGroup1andGroup2wasinjuredheavily,theinjuryinGroup3wasmild.ThedifferencesbetweenGroup1andGroup2werenotsignificant.ComparedwiththeratsinGroup1andGroup2,theonesinGroup3hadmoreclearlydemarcatedretinastructureandmoreorderedcellsbylightmicroscopeandTEMobservation.TheONLthicknesses(400times)offourgroupsateachtimepointexceptbetweenGroup1andGroup2weresignificantlydifferent(P<0.05).ThethicknessesoftheONLinGroup1atthreetimepointswere30.41±4.04μm,26.11±2.82μmand20.63±1.06μm,inGroup2were31.62±4.54μm,25.08±3.63μmand19.07±3.86μm,inGroup3were29.75±3.62μm,28.83±1.97μmand27.61±1.83μm.InGroup4themeanofthethicknesswas37.35±1.37μm.Astimewentby,thedamageg
简介:糖尿病视网膜病变(DR)是作为一种常见的糖尿病并发症,对其发病机制的研究一直是关注的焦点。经典的糖尿病视网膜病变的发病机制假说集中与多元醇通路的异常、蛋白质非酶糖基化产物的堆积、蛋白激酶C及氨基己糖途径有关。聚腺苷二磷酸核糖聚合酶(PARP)作为统一机制中的一个关键分子,与DR发病机制及其防治密不可分,对其进行适当干预,可成为DR治疗的重要方法之一。