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N-乙酰半胱氨酸对大鼠膀胱缺血/再灌注损伤的保护作用。

Protective effect of N-acetylcysteine against ischemia/reperfusion injury in rat urinary bladders.

机构信息

Department of Urology, School of Medicine, Chungnam National University Hospital, Daejeon, 301-721, Korea.

出版信息

Cell Biochem Funct. 2014 Jan;32(1):24-30. doi: 10.1002/cbf.2967. Epub 2013 Apr 16.

Abstract

Ischemia/reperfusion (I/R) injury represents an important cause of bladder contractile dysfunction. One of the major causes leading to this dysfunction is thought to be reactive oxygen species formation. In this study, we investigated the potential benefit of N-acetylcysteine (NAC), a potent antioxidant that neutralizes free radicals, in a rat model of urinary bladder injury. NAC treatment rescues the reduction of contractile response to I/R injury in a dose-dependent manner. In addition, all levels of reactive oxygen species, lipid peroxidation, and NADPH-stimulated superoxide production in the I/R operation+NAC (I/R+NAC) group also decreased compared with a marked increase in the I/R operation+saline (I/R+S) group. Moreover, an in situ fluorohistological approach also showed that NAC reduces the generation of intracellular superoxides enlarged by I/R injury. Together, our findings suggest that NAC has a protective effect against the I/R-induced bladder contractile dysfunction via radical scavenging property.

摘要

缺血/再灌注 (I/R) 损伤是膀胱收缩功能障碍的重要原因。导致这种功能障碍的主要原因之一被认为是活性氧物质的形成。在这项研究中,我们研究了 N-乙酰半胱氨酸 (NAC) 的潜在益处,NAC 是一种能够中和自由基的强效抗氧化剂,在大鼠膀胱损伤模型中具有治疗作用。NAC 治疗以剂量依赖的方式挽救了对 I/R 损伤收缩反应的降低。此外,与 I/R 操作+盐水 (I/R+S) 组的明显增加相比,I/R+NAC (I/R+NAC) 组的所有活性氧物质、脂质过氧化和 NADPH 刺激的超氧化物产生水平也降低。此外,原位荧光组织化学方法还表明,NAC 减少了由 I/R 损伤引起的细胞内超氧化物的产生。总之,我们的研究结果表明,NAC 通过清除自由基对 I/R 诱导的膀胱收缩功能障碍具有保护作用。

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