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作 者:李爱冬[1] 羊惠君[1] 韦纯义[2] 康健[3] 王凡
机构地区:[1]华西医科大学解剖教研室,成都610041 [2]华西医科大学附属第一医院眼科 [3]川北医学院解剖教研室
出 处:《中华眼底病杂志》1999年第3期157-159,共3页Chinese Journal of Ocular Fundus Diseases
基 金:华西医科大学校基金
摘 要:目的 观察1~16 周糖尿病大鼠视网膜血管内皮细胞(retinalvesselendothelialcells,RVECs)凋亡、增生特性的变化及p53 和bcl2的表达,探讨糖尿病视网膜病变(diabeticretinopathy,DR)的发病机制。 方法 用四氧嘧啶造Wistar大鼠糖尿病模型。视网膜血管行碳素墨水灌注,作视网膜铺片和切片、核苷酸末端转移酶介导dUTP缺口翻译法(TdTm ediated dUTPm ick end labelling m ethod,TUNEL法)和抗生物素蛋白生物素过氧化物酶复合物法(avidinbiotinperaxidase com plex,ABC)染色,光镜观察。 结果 1~16周糖尿病大鼠RVECs未见凋亡。与对照组大鼠视网膜相比,血管形态和结构无明显变化。第10~16周糖尿病大鼠RVECs呈增生细胞核抗原、5溴2脱氧核苷尿嘧啶、p53 和bcl2免疫反应阳性,但未见内皮细胞堆积和新生血管形成征象。对照组大鼠RVECs为阴性反应。 结论 1~16周糖尿病大鼠RVECs尚未发生凋亡和增生,但10周时已被激活进入细胞周期。p53和bcl2的表达可能对稳?Objective To observe apoptotic and proliferative characteristics of the retinal vascular endothelial cells(RVECs) of the 1~16 weeks diabetic rats and p53 and bcl 2 expressions of the rats,in order to probe the pathogenic mechanism of diabetic retinopathy(DR). Methods Models of diabetic Wistar rats were made by alloxan venous injection.The retinal blood vessels were filled by ink,the wholemounts and paraffin embedded sections of the retinas were made,TUNEL staining and Immunohistochemical ABC staining were used,and light microscopy was taken,in succession. Results Apoptosis of the RVECs was not found.Compared with control group,the morphologic features of the RVECs and the structure of the retinal blood vessels remained unchanged.In the period from the 10th to the 16th week,the immunohistochemical stain of PCNA,BrdU,p53,and bcl 2 for RVECs revealed positive results,but there was no any sign of the RVECs stacking and proliferating or new blood vessels forming in the retinas.In control group,the reaction of immunological stain of the aforementioned parameters was negative. Conclusions No accelerated apoptosis and proliferation of the RVECs in the 1~16 week diabetic rats happen after alloxan injection.Almost all of the RVECs were stimulated to enter the cell cycle in the 10th week.Expression of p53 and bcl 2 might play an important role in stabilizing the RVECs in early stage of diabetes.
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