期刊文献+

内毒素致家兔急性肺损伤及萘普生保护性作用的研究 被引量:3

Study on endotoxin-induced acute lung injury and antagonizing effects of naproxen in rabbits
下载PDF
导出
摘要 目的:探讨大肠杆菌内毒素(ET)致兔急性肺损伤(ALI)的发病机制及萘普生的干预作用。方法:24只大耳白兔随机均分为对照组(A组)、ET致伤组(B组)、ET致伤+萘普生处理组(C组)。颈静脉注射ET(600μg/kg)致兔ALI,监测动物动脉血气、血清和肺组织中TXB2和6-keto-PGF1α含量的变化。于4h处死动物,取肺组织观察病理变化及用免疫组化方法检查过氧化物酶增殖子活化受体γ(PPARγ)的表达情况。结果:与对照组相比,损伤组动物动脉血氧分压(PaO2)下降、血清及肺组织中TXB2和6-keto-PGF1α含量增加(P<0.01);肺组织出现明显的病理损害。萘普生处理组PaO2未见明显下降,血清及肺组织中TXB2和6-keto-PG1α值低于ET组;病理检查见轻度肺水肿,炎细胞浸润较ET组少。免疫组化见损伤组肺组织PPARγ表达明显下降,萘普生组好于损伤组。结论:静脉注射ET可复制兔ALI动物模型;环氧合酶(COX)在ALI时激活,PPARγ表达减少。萘普生可能通过抑制COX的活性和激活PPARγ对ALI有一定的干预作用。 Objective:To study the pathogenesis of endotoxin (ET)-induced acute lung injury(ALI) and the antagonizing effects of naproxen in rabbits. Methods: 24 Flap-eared white rabbits were randomly assigned to three groups: control group (group A), ET-treated group(group B) and combination group(treated by ET and naproxen, group C). ALI was induced by intravenous injection of ET(600 μg/kg) by jugular vein. During the experiment, arterial blood gases, the contents of TXB2 and 6-keto-PGFloin both serum and lung tissue were measured. When rabbits were killed at 4h of the experiment, the pathologic changes of pulmonary tissue were examined with light microscope, and Peroxiseme proliferator-activated receptor γ(PPARγ) were examined by immunohistochemistry. Results:Compared with group A, rabbits of group B showed PaO2 decreased, the contents of TXB2 and 6-keto-PGF1α increased in both serum and lung tissue (P 〈 0.01 ) ; the pathological examination showed obviously injury in pulmonary tissue;the contents of TXB2 and 6-keto-PGF1α in serum and lung tissue were lower in group C than those in group B. Pulmonary edema and inflammatory cell infiltration were obviously severe in group B compared with those seen in group C. The expression of pulmonary PPARγ in group C was better than that in group B. Conclusion:An intravenous injection of ET can reproduce ALI model in rabbits. Cylcooxygenase (COX) was activated during the period of ALI and it was an important factor in pathogenesis of ET-induced ALL The decreased PPARγ expression was found in ET-induced ALI. Naproxen had some protective effects to ET-induced ALI in rabbits by means of activating PPARγ and antagonizing COX activities.
出处 《军医进修学院学报》 CAS 北大核心 2006年第3期206-208,共3页 Academic Journal of Pla Postgraduate Medical School
关键词 萘普生 呼吸窘迫综合征 成人 内毒素类 过氧化物酶增殖子活化受体γ 动物 naproxen respiratory distress syndrome, adult endotoxins PPAR- gamma animal, rabbit
  • 相关文献

参考文献8

  • 1薛庆亮,汪建新,江宏.内毒素致兔急性肺损伤及1,6-二磷酸果糖保护性作用的研究[J].军医进修学院学报,2005,26(1):57-59. 被引量:6
  • 2江宏,汪建新,薛庆亮.内毒素致兔急性肺损伤及磷脂酶A_2致伤机制的研究[J].军医进修学院学报,2004,25(5):360-362. 被引量:7
  • 3Jiang C,Ting AT,See B.PPARγ agonists inhibit production of monocyte inflammatory cytokines[J].Nature,1998,391:82-86.
  • 4Kazuhiro A,Shigekazu S,Takafumi S,et al.Peroxisome proliferator-activated receptor γin human alveolar macrophages[J].Am J Respir Crit Car Med,2004,169(2):195-200.
  • 5Maisa SJ,Buanus W,Srichan P,et al.Activation of peroxisome proliferator-activated receptor isoformsand inhibition of prostaglandin H2 synthases by ibuprofen,naproxen and indomethacin[J].Bioc Pharm,2001,62:1587-1595.
  • 6Daniel P,Alan H,Stephensin,et al.Effect of eicosand inbibition on the development of pulmonary edema after acute lung injury[J].J Appl Physiol,1996,80(3):915-923.
  • 7Ito K,ShimadaJ,KatoD,etal.Protective effects of preischemic treatment with pioglitazone,a peroxisome proliferator-activated receptorγ ligand,on lung ischemia-reperfusion injury in rats[J].Eur J Cardiothorac Surg,2004,25 (4):530-536.
  • 8Mie M,Yukio I,Ken I,et al.Role of 15-Deoxy△12,14-prostaglandin J2and Nrf2Pathways in Protection against Acute Lung Injury[J].Am J Respir Crit Car Med,2005,171(11):1260-1266.

二级参考文献12

  • 1陈思锋,吴中立.体液和组织磷脂酶A_2简便快速测定法[J].第二军医大学学报,1989,10(3):254-256. 被引量:210
  • 2汪建新.急性肺损伤发病机理及治疗研究进展[J].国外医学(生理病理科学与临床分册),1996,16(2):114-116. 被引量:5
  • 3Nagase T, Uozumi N, Ishii S, et al. Acute lung injury by sepsis and acid aspiration: a key role for cytosolic phospholipase A2 [J].Nat Immunol, 2000, 1(1) : 42-46.
  • 4Nunes FB, Simoes-Pires MG, Farias-Alves-Filho JC, et al. Physiopatholoical studies in septic rats and the use of fructose 1,6-bisphosphate as cellulars protection [J]. Crit Care Med, 2002, 30(9) :2069-74.
  • 5Furue S, Kuwabara K, Mikawa K, et al. Crucial role of group ⅡA phospholipase A2 [J]. Am J Respir Crit Care Med, 1999, 160(4) : 1292-1302.
  • 6Tamaki T, Nakai T, Yamaue H, et al. Fructose-1,6-Bisphosphate inhibits excess activation of Kupffer cell function induced by endotoxin[J]. Dig Dis Sci, 2002, 47(10) : 2179-2185.
  • 7Vexler Z, Berrios M, Ursell PC, et al. Toxicity of fructose-1,6-bi-sphosphate in developing normoxic rats. Pharmacol Toxicol[J],1999, 84(3) : 115-121.
  • 8Bersten A D, Edibam C, Hunt T, et al. Incidence and mortality of acute lung injury and the acute respiratory distress syndrome in three Australian States[J]. Am J Respir Crit Care Med, 2002, 165(4): 443-448.
  • 9Nagase T, Uozumi N, Ishii S, et al. Acute lung injury by sepsis and acid aspiration: a key role for cytosolic phospholipase A2[J]. Nat Immunol, 2000 , 1(1): 42-46.
  • 10Furue S, Kuwabara K, Mikawa K, et al. Crucial role of group IIA phospholipase A2[J]. Am J Respir Crit Care Med, 1999, 160(4): 1292-1302.

共引文献9

同被引文献17

引证文献3

二级引证文献7

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