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富含脂质的饮食会加速阿霉素诱导的肾病中的肾小球硬化。

Glomerulosclerosis in adriamycin-induced nephrosis is accelerated by a lipid-rich diet.

作者信息

Song H, Li X, Zhu C, Wei M

机构信息

Department of Pediatrics, Peking Union Medical College (PUMC) Hospital, Chinese Academy of Medical Science (CAMS) and PUMC, Beijing 100730, China.

出版信息

Pediatr Nephrol. 2000 Dec;15(3-4):196-200. doi: 10.1007/s004670000464.

Abstract

The present study was performed to determine quantitatively the effect of hypercholesterolemia induced by a lipid-rich diet on glomerulosclerosis in an animal model of nephrotic syndrome (NS) induced by Adriamycin (ADR). Twenty NS Wistar rats administered ADR with a single intravenous dose of 5 mg/kg body weight were divided into standard and lipid-rich chow groups. Another 20 weight-matched non-NS rats that received a vehicle alone were grouped as controls. Quantitative analyses of renal histological changes were performed with determination of blood and urine biochemical parameters. It was found that serum cholesterol was markedly higher in rats with lipid-rich chow in both NS and non-NS rats. Urinary protein was significantly higher in rats on the lipid-rich diet in the NS group. The mesangial matrix and cell indices were significantly increased in rats with the lipid-rich diet and the most obvious changes were found in the NS group. Lipid deposits and foam cells were observed in mesangial areas, and some glomeruli had progressed to form focal and segmental glomerulosclerosis in the NS group. Findings indicated that diet-induced hyperlipidemia can lead to proliferation of mesangial cells and accumulation of mesangial matrices, and further aggravate glomerulosclerosis in Adriamycin-induced nephrosis.

摘要

本研究旨在定量确定富含脂质饮食诱导的高胆固醇血症对阿霉素(ADR)诱导的肾病综合征(NS)动物模型中肾小球硬化的影响。将20只单次静脉注射5mg/kg体重ADR的NS Wistar大鼠分为标准饮食组和富含脂质饮食组。另外20只体重匹配的仅接受赋形剂的非NS大鼠作为对照组。通过测定血液和尿液生化参数对肾脏组织学变化进行定量分析。结果发现,NS组和非NS组中,富含脂质饮食的大鼠血清胆固醇明显更高。NS组中,富含脂质饮食的大鼠尿蛋白明显更高。富含脂质饮食的大鼠系膜基质和细胞指数显著增加,且在NS组中变化最为明显。在系膜区域观察到脂质沉积和泡沫细胞,NS组中一些肾小球已进展为局灶节段性肾小球硬化。研究结果表明,饮食诱导的高脂血症可导致系膜细胞增殖和系膜基质积聚,并进一步加重阿霉素诱导的肾病中的肾小球硬化。

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