首页> 外文期刊>Journal of cardiovascular pharmacology and therapeutics >Curcumin attenuates cardiopulmonary bypass-induced lung oxidative damage in rats
【24h】

Curcumin attenuates cardiopulmonary bypass-induced lung oxidative damage in rats

机译:姜黄素减轻大鼠体外循环所致肺氧化损伤

获取原文
获取原文并翻译 | 示例
           

摘要

Objective: Acute lung injury is a common complication after cardiopulmonary bypass (CPB). Oxidative damage greatly impacts CPB-induced lung ischemic pathogenesis and may represent a target for treatment. We aimed to investigate whether curcumin upregulates heme oxygenase 1 (HO-1) expression and ameliorates lung injury in a rat CPB model. Methods: A total of 80 male Sprague-Dawley rats were divided into 2 sets of 5 groups (n = 8 per group): sham; control (CPB); vehicle; low-dose curcumin (L-Cur); and high-dose curcumin (H-Cur). Animals were pretreated with a single intraperitoneal injection of vehicle, L-Cur (50 mg/kg), or H-Cur (200 mg/kg) 2 hours prior to CPB. Lung tissue, serum, and bronchoalveolar lavage fluid was harvested 2 or 24 hours postoperatively. In the control group, CPB-induced lung injury was confirmed by histopathologic examination and a significantly increased wet-to-dry lung weight ratio and pulmonary permeability index value was observed (P < .05 vs sham group). Cardiopulmonary bypass was associated with a marked rise in the level of malondialdehyde and myeloperoxidase and a fall in superoxide dismutase 2 and 24 hours after surgery (P < .05 vs sham group). Administration of curcumin ameliorated lung damage and reversed the oxidative stress markers in a partially dose-dependent manner (P < .05 vs vehicle group). Furthermore, HO-1 gene transcription and protein expression were elevated to a greater extent in the lungs after curcumin pretreatment compared with the vehicle pretreatment. Conclusions: Curcumin has the potential to provide protection from CPB-induced lung damage reflected in the expression of oxidative stress markers. The antioxidant effect of curcumin may be partly related to upregulation of HO-1.
机译:目的:急性肺损伤是体外循环(CPB)后的常见并发症。氧化损伤极大地影响了CPB诱导的肺缺血的发病机制,可能代表了治疗的目标。我们旨在研究姜黄素是否在大鼠CPB模型中上调血红素加氧酶1(HO-1)的表达并改善肺损伤。方法:将80只雄性Sprague-Dawley大鼠分为两组,每组5组,每组8只。控制(CPB);车辆;低剂量姜黄素(L-Cur);和大剂量姜黄素(H-Cur)。在CPB前2小时,通过腹膜内注射媒介物,L-Cur(50 mg / kg)或H-Cur(200 mg / kg)对动物进行预处理。术后2或24小时收集肺组织,血清和支气管肺泡灌洗液。在对照组中,通过组织病理学检查证实了CPB诱导的肺损伤,并且观察到干湿肺重量比和肺通透性指数值显着增加(与假手术组相比,P <.05)。体外循环与术后2小时和24小时丙二醛和髓过氧化物酶水平的显着升高以及超氧化物歧化酶的下降相关(与假手术组相比,P <.05)。姜黄素的给药改善了肺损伤,并以部分剂量依赖性方式逆转了氧化应激标志物(与溶媒组相比,P <.05)。此外,与媒介物预处理相比,姜黄素预处理后肺中HO-1基因的转录和蛋白质表达水平更高。结论:姜黄素具有潜在的保护作用,可抵御CPB诱导的肺损伤,氧化应激标志物的表达反映了这一点。姜黄素的抗氧化作用可能与HO-1的上调有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号