首页> 中文期刊> 《中国老年学杂志》 >CORM-2对百草枯致老年小鼠肺纤维化的保护作用

CORM-2对百草枯致老年小鼠肺纤维化的保护作用

         

摘要

Objective To observe the protection effect of carbon monoxide releasing molecule-2 ( CORM-2) performed in aged mice pulmonary fibrosis induced by Paraquat (PQ) and its mechanism. Methods 72 aged mice were divided into sham, paraquat, CORM-2 + paraquat, iCORM-2 + paraquat groups, each group had 18 mice. Six mice from each group were killed randomly 3, 5 and 7 d post-drug administration, and artery blood, serum and lung tissues were harvested respectively, the level of arterial oxygen partial pressure between groups was analyzed, the serum level of TNF-ot and the lung tissues levels of MDA, MPO were analyzed by ELISA, the degree of lung injury was also analyzed by the lung tissue wet dry ratio and the protein level of BALF, the degree of pulmonary fibrosis between groups were contrasted by cellulose dyeing, inducible nitric oxide synthase (iNOS) level in lung tissues was analyzed by Western blot Results Compared with those of sham group, artery blood oxygen partial pressure was decreased and the lung tissue levels of MDA, MPO were increased, these changes in paraquat and iCORM-2 + paraquat groups were more apparent, but there were not significant differences between paraquat and iCORM-2 + paraquat groups. In CORM-2 + paraquat group, the lung injury and pulmonary fibrosis were alleviated, and had significant difference. Conclusions CORM-2 can protect lung injury of pulmonary fibrosis aged mice induced by paraquat, through suppressing oxidation activity by carbon monoxide. It also inhibits iNOS expression so as to improve lung function%目的 观察一氧化碳释放因子(CORM-2)对百草枯(Paraquat,PQ)诱导的老年小鼠肺纤维化的保护作用及其机制.方法 72只C57BL/6老年小鼠随机分为对照组、PQ组、CORM-2+ PQ组、iCORM-2+ PQ组,每组18只.之后分别在给药后3、5、7d处死小鼠,留取动脉血、血清及肺组织,分析各组之间动脉血氧分压差别;ELISA法检测血清TNF-α水平,检测肺组织湿干重比,肺组织特殊病理学染色对比各组之间肺纤维化变化,肺组织MDA、MPO水平变化,Western印迹分析肺组织一氧化氮合酶(iNOS)表达水平变化.结果 与对照组相比,其他各组小鼠动脉血氧分压下降,肺组织MDA、MPO升高,此变化在PQ组及iCORM-2+ PQ组中更为明显,而这两组无明显差别;在CORM-2+ PQ组中小鼠血氧饱和度下降较前两组明显改善,肺纤维化程度减轻,并具有显著性差异.结论 CORM-2对于PQ导致的老年小鼠肺纤维化具有保护作用,此保护作用可能与一氧化碳的抗氧化作用有关,并且可能通过抑制iNOS的表达而改善肺脏氧合功能.

著录项

  • 来源
    《中国老年学杂志》 |2012年第6期|1174-1176|共3页
  • 作者单位

    哈尔滨医科大学第一临床医学院ICU,黑龙江哈尔滨150001;

    哈尔滨医科大学第一临床医学院ICU,黑龙江哈尔滨150001;

    哈尔滨医科大学第一临床医学院ICU,黑龙江哈尔滨150001;

    哈尔滨医科大学第一临床医学院ICU,黑龙江哈尔滨150001;

    哈尔滨医科大学第一临床医学院ICU,黑龙江哈尔滨150001;

    哈尔滨医科大学第一临床医学院ICU,黑龙江哈尔滨150001;

    哈尔滨医科大学第一临床医学院ICU,黑龙江哈尔滨150001;

    哈尔滨医科大学第一临床医学院ICU,黑龙江哈尔滨150001;

  • 原文格式 PDF
  • 正文语种 chi
  • 中图分类 肺疾病;
  • 关键词

    一氧化碳释放因子; 肺纤维化; 百草枯; 一氧化氮合酶;

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