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己酮可可碱对高草酸尿症大鼠模型中与肾结晶形成相关的氧化肾细胞损伤的保护作用。

Protective effect of pentoxifylline on oxidative renal cell injury associated with renal crystal formation in a hyperoxaluric rat model.

机构信息

Department of Pediatric Surgery, Medical School, Abant Izzet Baysal University, Bolu, Turkey.

Department of Physiology, Medical School, Abant Izzet Baysal University, Bolu, Turkey.

出版信息

Urolithiasis. 2019 Oct;47(5):415-424. doi: 10.1007/s00240-018-1072-8. Epub 2018 Jul 6.

Abstract

The aim of the study is to investigate the effects of pentoxifylline (PTX) on the renal tubular cell injury and stone formation in a hyperoxaluric rat model induced by ethylene glycol and its possible underlying mechanisms. The study was performed with 30 male Wistar rats and randomized into three groups of teen. The sham-control (group 1) received only drinking water orally. The EG/untreated (group 2) received drinking water containing 0.75% EG for 4 weeks orally. The EG/PTX treated (group 3) received drinking water containing 0.75% EG for 4 weeks orally and PTX. Urine and blood were collected to determine some parameters. The kidneys were also removed for histological examination. Serum and urinary parameters were significantly improved in the EG/PTX treated. In the EG/PTX-treated group, the MDA, TOS and MPO activity reduced and the TAS, SOD, CAT and GSH-Px activities were increased markedly compared with the group 2. In urine of the group 2 rats, a large number of CaOx crystals were displayed and most tubules that contained crystals were dilated and showed degeneration, necrosis, and desquamation of the lining epithelium. Only few CaOx crystals were r in EG/PTX-treated animal's urine. Mild tissue damage was observed in PTX-treated rats. iNOS expression was significantly elevated in the group 2. In contrast, in the EG/PTX-treated group, eNOS expression in renal tubular epithelial cells was increased. Current study indicates that PTX may partially reduce renal tubular injury resulting from hyperoxaluria-induced oxidative and nitrosative stress.

摘要

本研究旨在探讨己酮可可碱(PTX)对乙二醇诱导的高草酸尿大鼠模型肾小管细胞损伤和结石形成的影响及其可能的机制。本研究采用 30 只雄性 Wistar 大鼠,随机分为 3 组,每组 10 只。假手术对照(第 1 组)仅口服饮用水。EG/未处理(第 2 组)口服含 0.75%EG 的饮用水 4 周。EG/PTX 处理(第 3 组)口服含 0.75%EG 的饮用水 4 周,同时给予 PTX。收集尿液和血液以测定一些参数。还切除肾脏进行组织学检查。血清和尿液参数在 EG/PTX 治疗组显著改善。与第 2 组相比,EG/PTX 治疗组 MDA、TOS 和 MPO 活性降低,TAS、SOD、CAT 和 GSH-Px 活性显著增加。在第 2 组大鼠的尿液中,大量 CaOx 晶体显示,大多数含有晶体的小管扩张并显示出变性、坏死和衬里上皮脱落。在 EG/PTX 治疗动物的尿液中只有少量 CaOx 晶体。在 PTX 治疗的大鼠中观察到轻度组织损伤。第 2 组 iNOS 表达显著升高。相比之下,在 EG/PTX 治疗组,肾小管上皮细胞中 eNOS 表达增加。本研究表明,PTX 可能部分减轻高草酸尿诱导的氧化应激和硝化应激引起的肾小管损伤。

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