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丙泊酚对大鼠肾缺血/再灌注损伤的影响。

Effects of propofol on renal ischemia/reperfusion injury in rats.

作者信息

Yang Shun, Chou Wei-Ping, Pei Ling

机构信息

Department of Anesthesiology, First University Hospital of China Medical University, Shenyang, Liaoning 110000;

出版信息

Exp Ther Med. 2013 Nov;6(5):1177-1183. doi: 10.3892/etm.2013.1305. Epub 2013 Sep 18.

Abstract

Renal ischemia/reperfusion injury (IRI) is a major cause of acute renal failure. The aim of this study was to investigate whether propofol pretreatment in a rat model protects kidney tissue against IRI. Thirty-two Wistar rats were equally divided into four groups: a sham-operated group, untreated renal IRI group, and low-dose (5 mg/kg) and high-dose (10 mg/kg) propofol-treated groups which were treated with propofol prior to the induction of IRI. The rats were subjected to renal ischemia by bilateral clamping of the pedicles for 50 min, followed by reperfusion. The low-dose and high-dose propofol treatment groups were pretreated via femoral vein injection with a propofol suspension prior to the induction of ischemia/reperfusion. The untreated IRI group showed significantly higher serum creatinine (SCr), blood urea nitrogen (BUN), interleukin 6 (IL-6), IL-8, tumor necrosis factor-α (TNF-α), and malondialdehyde (MDA) levels compared with the sham-operated rats. Superoxide dismutase (SOD) levels were significantly reduced following IRI; however, they significantly increased following propofol administration. Bone morphogenetic protein 2 (BMP2) levels were significantly increased in the propofol-treated groups compared with the untreated IRI group. These results suggest that propofol reduces renal oxidative injury and facilitates repair following IRI. Propofol may play a protective role by regulating BMP2 expression in renal IRI.

摘要

肾缺血/再灌注损伤(IRI)是急性肾衰竭的主要原因。本研究的目的是探讨在大鼠模型中丙泊酚预处理是否能保护肾组织免受IRI损伤。32只Wistar大鼠平均分为四组:假手术组、未治疗的肾IRI组、低剂量(5mg/kg)和高剂量(10mg/kg)丙泊酚治疗组,丙泊酚治疗组在IRI诱导前用丙泊酚进行治疗。通过双侧夹闭肾蒂50分钟使大鼠遭受肾缺血,随后进行再灌注。低剂量和高剂量丙泊酚治疗组在缺血/再灌注诱导前经股静脉注射丙泊酚混悬液进行预处理。与假手术大鼠相比,未治疗的IRI组血清肌酐(SCr)、血尿素氮(BUN)、白细胞介素6(IL-6)、IL-8、肿瘤坏死因子-α(TNF-α)和丙二醛(MDA)水平显著升高。IRI后超氧化物歧化酶(SOD)水平显著降低;然而,丙泊酚给药后SOD水平显著升高。与未治疗的IRI组相比,丙泊酚治疗组骨形态发生蛋白2(BMP2)水平显著升高。这些结果表明,丙泊酚可减轻肾氧化损伤并促进IRI后的修复。丙泊酚可能通过调节肾IRI中BMP2的表达发挥保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/3820756/5be44daaa665/ETM-06-05-1177-g00.jpg

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