期刊文献+

脓毒症大鼠急性肺损伤机制研究 被引量:3

Mechanism of Acute Pulmonary Injury in Rats with Sepsis
下载PDF
导出
摘要 目的探讨脓毒症大鼠急性肺损伤的机制。方法采用盲肠结扎穿孔术(CLP)建立大鼠脓毒症模型。健康成年雄性SD大鼠48只,随机分为假手术组、脓毒症组,每组24只。动物模型制备成功后,于术后3、12、24h检测肺组织匀浆标本黄嘌呤氧化酶(XO)、丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)含量。光学显微镜下观察肺组织病理改变。结果术后3、12、24h假手术组XO分别为(2.4±0.3)U/g、(2.3±0.5)U/g、(2.4±0.4)U/g,MDA为(15.7±2.7)nmol/mg、(15.2±2.9)nmol/mg、(15.6±2.6)nmol/mg,SOD为(58.8±8.0)U/mg、(58.1±10.1)U/mg、(58.7±9.5)U/mg,GSH-Px为(33.2±5.4)U/mg、(32.5±7.0)U/mg、(33.1±6.3)U/mg;脓毒症组XO分别为(4.2±0.6)U/g、(5.5±0.7)U/g、(5.7±0.5)U/g,MDA为(29.3±5.7)nmol/mg、(36.3±6.6)nmol/mg、(41.4±7.3)nmol/mg,SOD为(43.3±7.0)U/mg、(41.8±6.9)U/mg、(38.2±7.4)U/mg,GSH-Px为(27.9±4.0)U/mg、(26.4±3.9)U/mg、(24.3±3.3)U/mg。与假手术组比较,脓毒症大鼠肺组织XO、MDA含量显著升高,SOD、GSH-Px含量显著降低,差异有统计学意义(P<0.01)。结论脓毒症大鼠存在急性肺损伤,其机制可能与氧化应激相关。 Objective To investigate the mechanism of acute pulmonary injury in sepsis rats. Methods Colon ligation perforation was applied to rats to establish sepsis model. Forty-eight healthy adult male SD rats were ran-domly divided into sham group and sepsis group(n=24 in each group). At 3, 12, 24h after surgery, every 8 rats in each group were sacrificed to obtain lung tissue for determination of xanthine oxidase(XO), malonaldehyde(MDA), superoxide dismutase(SOD), and glutathione peroxidase(GSH-Px). Pathological changes of lung tissue was observed with light microscopy. Results At 3, 12, 24h after surgery in sham group, XO were 2.4±0.3U/g, 2.3±0.5U/g, and 2.4±0.4U/g, MDA were 15.7±2.7nmol/mg, 15.2±2.9nmol/mg, 15.6±2.6nmol/mg, SOD were 58.8±8.0U/mg, 58.1±10.1U/mg, 58.7±9.5U/mg, and GSH-Px were 33.2±5.4U/mg, 32.5±7.0U/mg, 33.1±6.3U/mg; in sepsis group, XO were 4.2±0.6U/g, 5.5±0.7U/g, and 5.7±0.5U/g, MDA were 29.3±5.7nmol/mg, 36.3±6.6nmol/mg, 41.4±7.3nmol/mg, SOD were 43.3±7.0U/mg, 41.8±6.9U/mg, 38.2±7.4U/mg, and GSH-Px were 27.9±4.0U/mg, 26.4±3.9U/mg, 24.3±3.3U/mg. Com-pared with sham group, the concentration of XO and MDA were significantly increased and SOD and GSH-Px were significantly decreased in sepsis group(P〈0.01). Conclusion Sepsis rats suffer from acute pulmonary injury, which may be related to oxidative stress.
出处 《浙江中西医结合杂志》 2015年第10期918-920,F0002,共4页 Zhejiang Journal of Integrated Traditional Chinese and Western Medicine
基金 浙江省中医药科技计划项目(No.2010ZA047) 浙江中医药大学附属第三医院院级医药卫生科技计划项目(No.ZS10ZA04)
关键词 大鼠 脓毒症 肺损伤 黄嘌呤氧化酶 丙二醛 超氧化物歧化酶 谷胱甘肽过氧化物酶 rats sepsis pulmonary injury xanthine oxidase malonaldehyde superoxide dismutase glutathione peroxidase
  • 相关文献

参考文献4

二级参考文献32

  • 1陆献成,刘志勇.血红素加氧酶-1的变化对肺缺血再灌注损伤大鼠肺组织细胞因子分泌的影响[J].现代医学,2007,35(3):198-201. 被引量:5
  • 2Levy MM, Fink MP, Marshal JC, et al. SCCM/ESJCM/ ACCP/ATS/SJS international sepsis definition conference[J]. Intensive Care Med, 2003,29 : 530-538.
  • 3Desbuards N, Hyvelin JM, Machet MC, et al. Heine oxygenase-1 inducer hemin attenuates the progression of remnant kidney model[J]. Nephron Exp Nephro1,2009,113:35-44.
  • 4Okamoto I, Abe M, Shibata K, etal. Evaluating the role of inducible nitric oxide synthase using a novel and selective inducible nitric oxide synthase inhibitor in septic lung injury produced by cecal ligation and puncture[J].Am J Resp Criti Care Med, 2000, 162 : 716-722.
  • 5Matute-Bello G, Frevert CW, Martin TR. Animal models of acute lung injury[J].Am J Physiol Lung Cell Mol Physiol,2008, 295(3): 379-399.
  • 6Ferrandiz ML, Devesa I. Inducers of heme oxygenase-1[J].Curr Pharm Des, 2008,14(5):473-486.
  • 7Wilks A. Heme oxygenase: evaluation, structure, and mechanism[J].Antioxide Redox Signal,2002,4:603-614.
  • 8Peterson S J, Frishman WH, Abraham NG. Targeting heine oxygenase: therapeutic implications for diseases of the cardiovascular system[J]. Cardiol Rev, 2009,17: 99-111.
  • 9Angus DC, Linde-Zwirble WT, Lidicker J, et al. Epidemiol-ogy of severe sepsis in theUnited States: analysis of inci-dence ,outcome, and associated costs of care [j]. Crit CareMed,2001,2(7) :1303-1310.
  • 10Wu L,Gokden N,Mayeux PR. Evidence for the role of reac-tive nitrogen species in polymicrobial sepsis-induced renalperitubular capillary dysfunction and tubular injury [J]. JAm Soc Nephrol,2007,18(6):1807-1815.

共引文献20

同被引文献66

引证文献3

二级引证文献10

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部