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目的研究代谢综合征大鼠的肾脏损伤及病理变化情况。方法将8周龄(体重130～170g)清洁级Wistar大鼠在福州总医院动物实验科适应性喂养2周后,随机分为两组即对照组和实验组,对照组5只给予以正常饲料(医大基础饲料)喂养,实验组10只给予以高脂高盐饲料(49%基础饲料+12%猪油+8%花生+1%麻油+10%鸡蛋+5%牛乳粉+15%黄豆粉+2%盐)喂养,两组均自由摄食,24周后确定大鼠模型是否成功(代谢综合征标准:中心性肥胖为核心,同时合并以下四项指标中的任何两项:①甘油三酯水平升高;②HDL-C水平降低;③血压升高;④空腹血糖升高)。将造模成功大鼠6只及对照组5只行血肌酐、血尿酸和24h尿蛋白定量检查,并行常规肾脏HE、PASM染色及电镜检查。结果实验组24h尿蛋白定量明显高于对照组(P<0.05),两组血肌酐、血尿酸无明显差别(P>0.05)。实验组大鼠肾脏肾小球、肾小管及肾间质不同程度的病理改变,主要表现有肾小球系膜区轻度扩大,系膜细胞及基质轻度增生,足细胞肿胀,足突融合较弥漫,毛细血管腔多处瘀血,部分区域脏、壁层细胞粘连,肾小球未见沉积物。肾小管无萎缩,部分上皮细胞肿胀,线粒体肿胀,嵴减少,细胞表面微绒毛减少。间质偶见少量淋巴细胞和中性粒细胞浸润。结论代谢综合征可引起肾脏损伤表现为24h尿蛋白增多,肾脏病理损害以肾小球损害特别是足细胞的损害更为明显。
Objective To study the renal damage and pathological changes in rats with metabolic syndrome. Methods Wistar rats aged 8 weeks (weighing 130-170 g) were randomly divided into two groups (control group and experimental group) and the control group (5 rats) fed with normal diet (Group I basic diet), the experimental group was given 10 high fat and salt diet (49% basal diet + 12% lard + 8% peanut + 1% sesame oil + 10% egg + 5% milk powder + 15% + 2% salt), both groups were fed freely, and the success of the rat model was determined after 24 weeks (Metabolic syndrome criteria: central obesity as the core, combined with any two of the following four indicators: ① triglycerides Level increased; ② HDL-C levels decreased; ③ elevated blood pressure; ④ fasting blood glucose). Serum creatinine, serum uric acid and urinary protein were measured in 6 rats and 5 rats in control group respectively. The kidneys were examined by HE and PASM staining and electron microscopy. Results The 24 h urinary protein in the experimental group was significantly higher than that in the control group (P <0.05). There was no significant difference between the two groups in serum creatinine and serum uric acid (P> 0.05). In the experimental group, pathological changes of glomerulus, tubule and renal interstitium were observed in different degrees in rats. The main manifestations were mild glomerular mesangial area, mild mesangial cells and matrix hyperplasia, podocyte swelling, More diffuse, multiple capillary capillaries stasis, some areas of dirty, parietal cell adhesion, no glomerular deposits. No renal tubular shrinkage, some epithelial cells swelling, mitochondria swelling, crest reduction, cell surface microvilli reduced. Interstitial occasionally a small amount of lymphocytes and neutrophil infiltration. Conclusions Metabolic syndrome can cause kidney damage in 24 hours with increased urinary protein. The damage of renal pathology is more obvious in glomerular damage, especially podocyte.