首页> 外文期刊>American Journal of Physiology >Skeletal muscle reperfusion injury is enhanced in extracellular superoxide dismutase knockout mouse.
【24h】

Skeletal muscle reperfusion injury is enhanced in extracellular superoxide dismutase knockout mouse.

机译:骨骼肌再灌注损伤在细胞外超氧化物歧化酶敲除小鼠中增强。

获取原文
获取原文并翻译 | 示例
           

摘要

This study investigates the role of extracellular SOD (EC-SOD), the major extracellular antioxidant enzyme, in skeletal muscle ischemia and reperfusion (I/R) injury. Pedicled cremaster muscle flaps from homozygous EC-SOD knockout (EC-SOD-/-) and wild-type (WT) mice were subjected to 4.5-h ischemia and 90-min reperfusion followed by functional and molecular analyses. Our results revealed that EC-SOD-/- mice showed significantly profound I/R injury compared with WT littermates. In particular, there was a delayed and incomplete recovery of arterial spasm and blood flow during reperfusion, and more severe acute inflammatory reaction and muscle damage were noted in EC-SOD-/- mice. After 90-min reperfusion, intracellular SOD [copper- and zinc-containing SOD (CuZn-SOD) and manganese-containing (Mn-SOD)] mRNA levels decreased similarly in both groups. EC-SOD mRNA levels increased in WT mice, whereas EC-SOD mRNA was undetectable, as expected, in EC-SOD-/- mice. In both groups of animals, CuZn-SOD protein levelsdecreased and Mn-SOD protein levels remained unchanged. EC-SOD protein levels decreased in WT mice. Histological analysis showed diffuse edema and inflammation around muscle fibers, which was more pronounced in EC-SOD-/- mice. In conclusion, our data suggest that EC-SOD plays an important role in the protection from skeletal muscle I/R injury caused by excessive generation of reactive oxygen species.
机译:这项研究调查了主要的细胞外抗氧化酶细胞外SOD(EC-SOD)在骨骼肌缺血和再灌注(I / R)损伤中的作用。纯合EC-SOD基因敲除(EC-SOD-/-)和野生型(WT)小鼠的带蒂睾丸肌皮瓣进行4.5小时缺血和90分钟再灌注,然后进行功能和分子分析。我们的结果表明,与WT同窝仔相比,EC-SOD-/-小鼠表现出明显的I / R损伤。特别地,在再灌注期间动脉痉挛和血流恢复延迟且不完全,并且在EC-SOD-/-小鼠中注意到更严重的急性炎症反应和肌肉损伤。再灌注90分钟后,两组的细胞内SOD [含铜和锌的SOD(CuZn-SOD)和含锰的(Mn-SOD)] mRNA的水平均相似地下降。 WT小鼠中EC-SOD mRNA水平升高,而EC-SOD-/-小鼠中EC-SOD mRNA却无法检测到。在两组动物中,CuZn-SOD蛋白质水平降低,而Mn-SOD蛋白质水平保持不变。 EC-SOD蛋白水平在野生型小鼠中下降。组织学分析显示肌肉纤维周围有弥漫性水肿和炎症,这在EC-SOD-/-小鼠中更为明显。总而言之,我们的数据表明EC-SOD在保护骨骼肌I / R损伤中起重要作用,而骨骼肌I / R损伤是由过量活性氧产生引起的。

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