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机构地区:[1]辽宁医学院第一附属医院眼科,辽宁省锦州市121000
出 处:《眼科新进展》2010年第4期328-331,共4页Recent Advances in Ophthalmology
基 金:辽宁省教育厅科学技术研究项目基金资助(编号:2008404)~~
摘 要:目的探讨果糖二磷酸镁(magnesium fructose diphosphata,FDPMg)对实验性大鼠视网膜缺血再灌注损伤的影响及其作用机制。方法通过升高眼压的方法,制作大鼠实验性视网膜缺血再灌注损伤的模型。将66只SD大鼠随机分为正常组、缺血再灌注模型组、FDPMg干预组。后两组各分为6h、12h、24h、48h、72h5个时间段。采用DNA原位末端标记法检测凋亡的视网膜细胞;免疫组织化学法检测视网膜组织中Fas/FasL蛋白的表达变化。结果正常组大鼠视网膜未见凋亡细胞。缺血再灌注模型组再灌注6h可观察到凋亡细胞;12h凋亡细胞逐渐增加;24h细胞凋亡达高峰;48h凋亡细胞减少;72h视网膜仍可见凋亡细胞。各组Fas/FasL表达情况与视网膜细胞凋亡情况基本一致。FDPMg干预组各时段各观察指标表达均较缺血再灌注模型组明显下降,两组间比较差异均有显著统计学意义(均为P<0.01)。结论FD-PMg明显抑制Fas/FasL蛋白在视网膜缺血再灌注损伤中的表达,进而抑制细胞凋亡来实现其对视网膜缺血再灌注损伤的保护作用。Objective To investigate the protective effect of magnesium fructose diphosphata(FDPMg)on retinal ischemical reperfusion injury and its mechanisms in experimental mice.Methods The models of retinal ischemical reperfusion injury were made by elevating intraocular pressure.A total of 66 SD rats were randomly divided into normal control group,ischemical reperfusion model group and FDPMg treatment group.The latter two groups were subdivided into 6 hours,12 hours,24 hours,48 hours and 72 hours after reperfusion groups.DNA in situ end labeling(terminal dUTP nick end labelling,TUNEL)was used to detect apoptotic retinal cells;Immunohistochemical method was used to measure changes of Fas/FasL protein levels in retinal tissues.Results No apoptotic cells was found in normal control group.At the ischemical reperfusion model group,apoptotic cells were found at 6 hours after reperfusion,gradually increased at 12 hours after reperfusion,went to peak at 24 hours after reperfusion,decreased at 48 hours after reperfusion and were still found at 72 hours after reperfusion.The expression of Fas/FasL was basically consistent with the condition of retinal cell apoptosis in each group.All observing indices in FDPMg treatment group were obviously lower than those in ischemical reperfusion model group,and there was significant difference(All P0.01).Conclusions FDPMg can obviously inhibit the expression of Fas/FasL protein during ischemical reperfusion injury,and further inhibit cell apoptosis to achieve its protective effect on retinal ischemical reperfusion injury.
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