CAJ | 학술논문

目的研究高胆固醇血症对雄性Wistar大鼠肾脏的毒性作用。方法用5％胆固醇饲料喂养雄性Wistar大鼠，制备高胆固醇动物模型，分别于实验第30、60和90 d测定肾功能、24 h尿蛋白、肾皮质胆固醇(Ch)及各磷脂含量，并进行病理形态及组织定量分析。结果在实验周期内实验组(E组)大鼠血浆肌酐水平无显著变化；第90 d，E组24 h尿微量白蛋白、肾皮质Ch、磷脂酰胆碱(PC)及磷脂酰乙醇胺(PE)显著高于正常对照组(C组)；病理形态及组织定量分析显示肾小球系膜细胞增生、炎性细胞浸润、系膜基质增多、毛细血管塌陷、上皮细胞足突融合，肾小球体积增大。IgG直接免疫荧光阴性，肾小球内无电子致密物沉积。相关分析显示肾小球体积、肾皮质Ch含量及24 h尿微量白蛋白排泄率等与血浆总胆固醇(TCh)及低密度脂蛋白(LDL)浓度呈显著正相关关系。结论饮食诱导的高胆固醇血症可导致Wistar大鼠肾毒性损伤。
목적 연구고담고순혈증대웅성Wistar대서신장적독성작용。방법 용5％담고순사료위양웅성Wistar대서，제비고담고순동물모형，분별우실험제30、60화90 d측정신공능、24 h뇨단백、신피질담고순(Ch)급각린지함량，병진행병리형태급조직정량분석。결과재실험주기내실험조(E조)대서혈장기항수평무현저변화；제90 d，E조24 h뇨미량백단백、신피질Ch、린지선담감(PC)급린지선을순알(PE)현저고우정상대조조(C조)；병리형태급조직정량분석현시신소구계막세포증생、염성세포침윤、계막기질증다、모세혈관탑함、상피세포족돌융합，신소구체적증대。IgG직접면역형광음성，신소구내무전자치밀물침적。상관분석현시신소구체적、신피질Ch함량급24 h뇨미량백단백배설솔등여혈장총담고순(TCh)급저밀도지단백(LDL)농도정현저정상관관계。결론 음식유도적고담고순혈증가도치Wistar대서신독성손상。
Purpose To Investigate the effect of diet-induced hyperchole sterolemia on the kidney ofWistar rats. Methods Male Wistar rats were fed with normal chow supplemented with 5 % cholesteroland observed biochemical changes in plasma lipid concentration, urinary microalbumin excretion, renalfunction, lipid component in renal cortices and morphological changes at 30,60 and 90 days. ResultsTotal plasma cholesterol (TCh) and low density lipoprotein (LDL) concentration were significantly elevatedin the group E (P＜0.05)at 30 days, and progressively increased thereafter, but during the entire study,there ere no differences in plasma urea nitrogen(BUN),creatinine(Cr), and endogenous creatinine clearance(Ccr) between the two groups. Quantitative urinary microalbumin excration was markely elevated in group E( P ＜ 0.05 ). Cholesterol (Ch), phosphatidylcholine(PC) and phosphatidylethanolamine(PE) levels of t he renalcortices were sigificantly increased in the group E at 12 weeks. Progressive development in mesangialhypercellulary, increased mesangial matrix, glomerular capillaries collapes were observed in the group E. Noelectron dense deposits were observed in any of the glomeruli examined. There was a siginificant positivecorrelation for the urinary microalbumin, Ch in the renal corticres, and glomerular size with plasma TCh andLDL concentration. Conclusions The diet-induced hypercholesterolemia may cause lipid nephrotoxicity inWistar rats.