首页> 外文期刊>The Tohoku Journal of Experimental Medicine >The protective effects of amifostine on adriamycin-induced acute cardiotoxicity in rats.
【24h】

The protective effects of amifostine on adriamycin-induced acute cardiotoxicity in rats.

机译:氨磷汀对阿霉素诱导的大鼠急性心脏毒性的保护作用。

获取原文
获取原文并翻译 | 示例
           

摘要

Free oxygen radicals and lipid peroxidation are responsible for adriamycin-induced cardiotoxicity. Amifostine is a scavenger of free radicals and may function as a selective cytoprotective agent. The aim of this study was to investigate the effects of amifostine on adriamycin-induced lipid peroxidation and the levels of protective enzymes in the heart. Male Wistar rats were randomly allocated to three groups: pretreated, untreated, and control (n=10 in each group). Rats were pretreated with an intraperitoneal injection of amifostine (200 mg/kg) 30 min before the injection of adriamycin. The pretreated rats were given an intraperitoneal injection of adriamycin (10 mg/kg) and were sacrificed after 72 h. Likewise, rats received intraperitoneal injection of adriamycin (untreated) or saline (control). The hearts were removed for the analyses of malondialdehyde (MDA), reduced glutathione (GSH) and catalase. MDA levels were increased (p<0.005) in the heart tissues of untreated rats compared to control, while GSH and catalase levels were decreased (p<0.05 and p<0.001, respectively) in untreated animals. In amifostine-preatreated group, MDA levels were lower (p<0.01), and GSH and catalase levels were higher (p<0.05 for both) than the untreated group. GSH levels were even higher in the amifostine-pretreated group compared to control (p<0.01), although catalase levels were significantly lower in the pretreated group (p<0.05). These results indicate that amifostine decreases adriamycin-induced lipid peroxidation and increases the levels of the protective enzymes in the heart tissue. Therefore, amifostine may ameliorate the adriamycin-induced acute cardiotoxicity.
机译:游离氧自由基和脂质过氧化作用是阿霉素诱导的心脏毒性的原因。氨磷汀是自由基的清除剂,可以用作选择性细胞保护剂。这项研究的目的是研究氨磷汀对阿霉素诱导的脂质过氧化作用和心脏保护酶水平的影响。将雄性Wistar大鼠随机分为三组:预处理组,未处理组和对照组(每组n = 10)。在注射阿霉素前30分钟,以腹膜内注射氨磷汀(200 mg / kg)对大鼠进行预处理。给予预处理的大鼠腹膜内注射阿霉素(10 mg / kg),并在72 h后处死。同样,大鼠接受腹腔注射阿霉素(未治疗)或生理盐水(对照)。取出心脏进行丙二醛(MDA),还原型谷胱甘肽(GSH)和过氧化氢酶的分析。与对照组相比,未经治疗的大鼠心脏组织中的MDA水平升高(p <0.005),而未经治疗的动物中GSH和过氧化氢酶水平降低(分别为p <0.05和p <0.001)。氨磷汀预处理组的MDA水平低于未治疗组(p <0.01),GSH和过氧化氢酶水平较高(两者均p <0.05)。氨磷汀预处理组的GSH水平甚至高于对照组(p <0.01),尽管过氧化氢酶水平明显低于对照组(p <0.05)。这些结果表明,氨磷汀可降低阿霉素诱导的脂质过氧化作用并增加心脏组织中保护酶的水平。因此,氨磷汀可以减轻阿霉素引起的急性心脏毒性。

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