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氧自由基在阿霉素诱导的肾病中的作用。

Role of oxygen radicals in adriamycin-induced nephrosis.

作者信息

Wu S H, Yang Y C, Wang Z M

机构信息

Department of Pediatrics, First Affiliated Hospital of Nanjing Medical College.

出版信息

Chin Med J (Engl). 1990 Apr;103(4):283-9.

PMID:2118039
Abstract

The mechanism of cellular processes responsible for proteinuria induced by adriamycin (ADR) remains unclear. In this study, we examined whether oxygen radicals contribute to the development of proteinuria in ADR-induced nephrosis. The peak concentration of malondialdehyde (MDA) of kidney was found on 8th day after ADR treatment in rats. ADR-treated rats received either superoxide dismutase (SOD, scavenger of O2-, catalase (CAT, scavenger of . H2O2) or dimethyl sulfoxide (DMSO, scavenger of OH). The SOD, CAT or DMSO treated groups had a significant suppression of urinary protein excretion, serum and renal MDA compared to ADR control group. There were also less severe renal morphologic changes in the former three groups vs the ADR controls. These data provide indirect evidence that oxygen radicals generated by ADR are important mediators of ADR-induced proteinuria.

摘要

阿霉素(ADR)诱导蛋白尿的细胞过程机制尚不清楚。在本研究中,我们检测了氧自由基是否在ADR诱导的肾病蛋白尿发展中起作用。大鼠接受ADR治疗后第8天,肾脏丙二醛(MDA)浓度达到峰值。接受ADR治疗的大鼠分别给予超氧化物歧化酶(SOD,O2-清除剂)、过氧化氢酶(CAT,.H2O2清除剂)或二甲基亚砜(DMSO,OH清除剂)。与ADR对照组相比,SOD、CAT或DMSO治疗组的尿蛋白排泄、血清和肾脏MDA均有显著抑制。与ADR对照组相比,前三组的肾脏形态学变化也较轻。这些数据提供了间接证据,表明ADR产生的氧自由基是ADR诱导蛋白尿的重要介质。

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