高脂饮食诱导大鼠肾损伤及其氧化应激水平的研究

目的:观察高脂饮食诱导健康Wistar大鼠的脂质肾毒性损伤及其氧化应激水平的变化,探讨氧化应激机制在其中的作用。方法:健康Wistar雄性大鼠16只,随机分为普通饲料组与高脂饲料组。普通饲料含热能308.98kcal/100g,高脂饲料在普通饲料基础上,添加20%猪板油,10%白砂糖,0.1%胆盐(w/w),含热能475.67kcal/100g。于实验第14周测定24h尿微量白蛋白、血脂、血糖并取肾组织检测羰基化蛋白和丙二醛(MDA)含量,并对肾脏病理形态学改变进行分析。结果:在14周时,高脂饲料组大鼠24h尿微量白蛋白、血脂以及肾组织羰基化蛋白和MDA含量明显高于普通饲料组(均P<0.01);病理形态学分析显示有肾小球球囊扩张、肾小球基底膜增厚、肾小球外系膜基质增生及肾小球局灶性节段性硬化;但2组大鼠空腹血糖、体质量及血清肌酐水平与普通饲料组相比差异无显著性(均P>0.05)。结论:高脂饮食诱导的高脂血症可导致健康大鼠的脂质肾毒性损伤,氧化应激很可能在其中发挥重要的作用。

Investigation of the High Fat Diet-Induced Renal Lesions of Healthy Rats and the Mechanism of Oxidative Stress

Objective:To investigate whether high fat diet can induce lipid nephrotoxicity in healthy wistar rats and the changes of oxidative stress level in high fat diet-induced renal lesions.Methods:16 healthy male Wistar rats were randomly divided into 2 groups:Group NC received standard laboratory chow diet.Group HF were fed with high fat diet to prepare the animal model of lipid nephrotoxicity. At the end of a 14-week period,detecting the biochemical index of renal function,urinary microalbumin excretion,plasma lipid concentration,fasting plasma glucose and contents of carbonyl protein,malondialdehyde (MDA) in renal cortex.Meanwhile,the morphological alteration of kidney was analyzed by image analysis system.Results:After high-fat feeding for 14 weeks,rats from group high fat diet developed hyperlipemia and albuminuria,which associated with significant increase(P<0.01) in contents of carbonyl protein,MDA in kidney tissue.In addition,pathomorphology changes of nephridial tissue were emerging: dilation of glomerular saccule,proliferation of extracellular matrix and focal segmental sclerosis of glomerulus.Conclusions:The high fat diet-induced hyperlipemia can cause lipid nephrotoxicity in healthy rats,in which oxidative stress potentially plays an important role.