摘要
目的:探讨肾小球足细胞裂隙膜蛋白podocin对足细胞形态及蛋白尿的影响。方法:32只体重160g～220g的雄性SD大鼠按阿霉素给药剂量随机分成小剂量组(3．0mg/Kg)、肾病剂量组(7．5mg/Kg)、超剂量组(10．0mg/Kg)、正常对照组。于给药第三周末处死大鼠,用氯化苄乙氧铵比浊法检测大鼠24h尿蛋白量,用免疫胶体金电镜检测大鼠肾小球蛋白podocin的表达和足细胞形态。结果:阿霉素组大鼠24h尿蛋白排泄量明显高于正常对照组,尤以肾病组最明显(P＜0．05);正常对照组大鼠podocin分布在靠近肾小球基底膜(GBM)的足突基底部,主要定位于裂隙隔膜的胞质面,部分金颗粒也可发现于GBM稍远的足突细胞表面．肾病组肾小球足突广泛融合,免疫胶体金颗粒几乎见不到;超剂量组和小剂量组podocin分布在靠近肾小球基底膜(GBM)的足突基底部,免疫胶体金颗粒数明显少于正常对照组,有部分足突退缩。结论:(1)podocin表达减少或消失可能是导致肾小球足突细胞融合的关键因素(2)蛋白尿的发生与肾小球足细胞裂隙膜蛋白podocin的减少或缺失有关。
Objective： To explore the effect of podocin on glomerular podocyte and its possible role in albuminuria occuring in nephropathy. Methods： Thirty two male SD rats （ weight from 160 to 220g） were enrolled in this study.They were randomly divided into the low dose group （injected with adriamycin （ADR） 3.0mg/Kg）, nephritic group （ adriamycin （ADR） 7,5mg/ Kg）, overdose group（adriamycin （ADR） 10.0mg/Kg） and normal control group（0.9% saline）. Three weeks after the injection, the excretion of 24 hours urinary protein of all rats was detected, meanwhile all rats were sacrificed and their renal cortexes were taken for localization. Immuno-gold electron microscopy was employed to study the distribution and quantitation of glomerular expres- sion of podocin, Results： The 24-hour urinary protein in control group was 7,98±3.01, Compared with control group,the levels of 24-hour urinary protein in ADR-treated groups were increased （14.35±9,72, 14,42±8,57 ）, especially in nephritic group （88.46± 23.52, P （0,05）. Podocin in control group distributed at the base of the podocyte foot processes near the GBM, It was primarily located at the cytoplasmic face of the plasmamembrane adjacent to the filtration shts,Small clusters of parfides of podocin were occa- sionally found along the surface of the foot processes with a distance from the GBM; In nephritic groups, No significant labelling was observed ,podocyte foot process confluenced; Compared with control group, the number of gold partide was obviously decreased, ,podocyte foot process were retraction in low-dose and overdose groups. Conclusion： （1） The reduction or disappearance of podocin in glomenflar podocyte slit diaphragm was the key factor to cause podocyte foot process confluence, （2） The decreased expresion of podocin and its abnormal distribution were closely associafied with the development of albuminuria.
出处
《现代生物医学进展》
CAS
2007年第6期863-864,848,共3页
Progress in Modern Biomedicine
