Sulforaphane Attenuates Contrast-Induced Nephropathy in Rats via Nrf2/HO-1 Pathway.
Sulforaphane Attenuates Contrast-Induced Nephropathy in Rats via Nrf2/HO-1 Pathway.
复制标题
萝卜硫素通过 Nrf2/HO-1 通路减轻大鼠造影剂肾病
DOI：
10.1155/2016/9825623
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发表时间：
2016
影响因子：
--
通讯作者：
Zou H
中科院分区：
文献类型：
--
作者：
Zhao Z;Liao G;Zhou Q;Lv D;Holthfer H;Zou H
背景。氧化应激在造影剂肾病（CIN）的发病机制中起重要作用。本研究的目的是探讨萝卜硫素（SFN）在大鼠CIN模型和HK2细胞氧化应激模型中的抗氧化作用。方法。将大鼠随机分为4组（每组n = 6）：对照组、Ioversol组（Ioversol诱导的CIN）、Ioversol + SFN组（SFN预处理的CIN大鼠）和SFN组（SFN处理的大鼠）。测定肾功能、丙二醛（MDA）和活性氧（ROS）。Western blot、实时聚合酶链反应、免疫组织化学检测核因子-红细胞衍生2-样2 （Nrf2）和血红素加氧酶-1 （HO-1）。结果。对比剂暴露后血清尿素氮（BUN）、肌酐和肾组织丙二醛（MDA）升高。与Ioversol组相比，Ioversol + SFN组血清BUN、肌酐和肾组织MDA均降低。SFN增加了CIN大鼠和ioversol诱导的HK2细胞中Nrf2和HO-1的表达。SFN提高了体外细胞活力，降低了ROS水平。结论。SFN在体外和体内均能减弱实验性CIN。这种作用可能激活Nrf2抗氧化防御途径。
Background. Oxidative stress plays an important role in the pathogenesis of contrast-induced nephropathy (CIN). The aim of this study was to investigate the antioxidant effects of sulforaphane (SFN) in a rat model of CIN and a cell model of oxidative stress in HK2 cells. Methods. Rats were randomized into four groups (n = 6 per group): control group, Ioversol group (Ioversol-induced CIN), Ioversol + SFN group (CIN rats pretreated with SFN), and SFN group (rats treated with SFN). Renal function tests, malondialdehyde (MDA), and reactive oxygen species (ROS) were measured. Western blot, real-time polymerase chain reaction analysis, and immunohistochemical analysis were performed for nuclear factor erythroid-derived 2-like 2 (Nrf2) and heme oxygenase-1 (HO-1) detection. Results. Serum blood urea nitrogen (BUN), creatinine, and renal tissue MDA were increased after contrast exposure. Serum BUN, creatinine, and renal tissue MDA were decreased in the Ioversol + SFN group as compared with those in the Ioversol group. SFN increased the expression of Nrf2 and HO-1 in CIN rats and in Ioversol-induced injury HK2 cells. SFN increased cell viability and attenuated ROS level in vitro. Conclusions. SFN attenuates experimental CIN in vitro and in vivo. This effect is suggested to activate the Nrf2 antioxidant defenses pathway.