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依达拉奉可预防大鼠膀胱缺血/再灌注诱导的功能和生化变化。

Edaravone protects against ischemia/reperfusion-induced functional and biochemical changes in rat urinary bladder.

作者信息

Matsumoto Seiji, Hanai Tadashi, Yoshioka Nobuhiro, Shimizu Nobutaka, Sugiyama Takahide, Uemura Hirotsugu, Levin Robert M

机构信息

Department of Urology, Kinki University School of Medicine, Osaka-Sayama, Osaka, Japan.

出版信息

Urology. 2005 Oct;66(4):892-6. doi: 10.1016/j.urology.2005.04.035.

Abstract

OBJECTIVES

To investigate the effects of edaravone on ischemia/reperfusion (I/R) injury in the rat bladder. Increasing evidence has shown that I/R are major etiologic factors in the progression of bladder dysfunction induced by partial outlet obstruction, and that part of the damage is due to the generation of free radicals. Edaravone is a newly developed radical scavenging agent that has been used for protection against I/R injury in patients with cerebral infarction.

METHODS

Thirty-five adult male rats were divided into five groups. Groups 1 to 4 underwent 1 hour of ischemia followed by 1 hour of reperfusion. Groups 1 to 3 were treated with edaravone at 1, 3, or 10 mg/kg body weight and group 4 with saline. Group 5 consisted of age-matched control rats. In vivo ischemia was created by clamping the vesical arteries for 1 hour. Reperfusion was accomplished by removing the clips and also lasted for 1 hour. Edaravone or saline was administered into the femoral artery after reperfusion for 30 minutes. After reperfusion, the bladder was excised and separated. The responses to electrical field stimulation, carbachol, and KCl were recorded. Other materials were analyzed for malondialdehyde as a measure of lipid peroxidation.

RESULTS

Edaravone administration resulted in protection of the contractile responses to both field stimulation and carbachol, although the responses to KCl were not affected. I/R resulted in an increase in malondialdehyde, which was reduced to control levels by edaravone.

CONCLUSIONS

These results suggest that edaravone has a potential protective effect against I/R-induced damage in the rat bladder.

摘要

目的

研究依达拉奉对大鼠膀胱缺血/再灌注(I/R)损伤的影响。越来越多的证据表明,I/R是部分出口梗阻所致膀胱功能障碍进展的主要病因,且部分损伤是由自由基生成引起的。依达拉奉是一种新开发的自由基清除剂,已用于保护脑梗死患者免受I/R损伤。

方法

35只成年雄性大鼠分为五组。第1至4组经历1小时缺血,随后1小时再灌注。第1至3组分别用1、3或10mg/kg体重的依达拉奉治疗,第4组用生理盐水治疗。第5组由年龄匹配的对照大鼠组成。通过夹闭膀胱动脉1小时造成体内缺血。通过移除夹子实现再灌注,再灌注也持续1小时。再灌注30分钟后,将依达拉奉或生理盐水注入股动脉。再灌注后,切除并分离膀胱。记录对电场刺激、卡巴胆碱和氯化钾的反应。分析其他材料中的丙二醛,作为脂质过氧化的指标。

结果

给予依达拉奉可保护对电场刺激和卡巴胆碱的收缩反应,尽管对氯化钾的反应未受影响。I/R导致丙二醛增加,依达拉奉将其降至对照水平。

结论

这些结果表明,依达拉奉对大鼠膀胱I/R诱导的损伤具有潜在的保护作用。

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