期刊文献+

硫氧还蛋白及其还原酶在新生鼠高氧肺损伤中的表达

Expression of thioredoxin and thioredoxin reductase in hyperoxia-induced lung injury of newborn rats
原文传递
导出
摘要 目的研究硫氧还蛋白(Trx)及其还原酶(TR)在早产新生鼠高氧肺损伤的肺组织中的表达变化及意义。方法早产新生SD大鼠,生后第一天随机分为空气组和高氧组,每组64只。两组分别于高氧或空气暴露后第4、7、10、14天提取肺组织总RNA,采取半定量逆转录聚合酶链反应(RT-PCR)测定Trx和TR mRNA表达;同时采用HE染色观察肺组织病理学变化,并进行辐射状肺泡计数(RAC)。结果病理学观察显示:与对照组比较,高氧组肺组织出现明显肺泡炎性改变和肺发育滞后,同时RAC值亦较空气组显著减少(P〈0.05)。高氧暴露各组Trx、TR mRNA表达较空气组均明显增强(P〈0.05),且二者表达强度分别于第10天和第7天达高峰。结论高氧上调肺组织Trx、TR表达;肺组织Trx系统表达增高可能在早产鼠高氧肺损伤的发病过程中发挥重要保护作用。 Objective To investigate the changes and potential roles of the expression of thioredoxin and thioredoxin reductase in the premature newborn rat lung exposed to hyperoxia. Methods On the first day after delivery, the preterm SD rats were randomly divided into air group and hyperoxia group (both n = 64). The rats were killed on day 4, 7, 10 and 14 respectively. Total RNA of lung was isolated and Trx and TR mRNA expression levels were detected by reverse transcription polymerase chain reaction( RT-PCR). The sections of lung were stained with HE method in order to assess lung histologic changes and examine lung radical alveolar counts (RAC). Results Rats in hyperoxia group showed typical lung injury, which was characterized by alveolitis and delay of lung development. Compared with air group, RACs were significantly decreased in hyperoxia group ( P 〈 0.05 ). RT-PCR results showed Trx and TR mRNA expression levels in hyperoxia group markedly increased, peaking at day 10 ( 1. 444 ± 0.142 vs 0. 609 ± 0. 078, P 〈 0.01 ) and day 7 (2. 035 ± 0. 160 vs 1. 325 ± 0.164, P 〈 0.01 ) respectively. Conclusion Trx and TR expression could be induced by hyperoxia, which might play an importantly protective role in the development of hyperoxia-induced lung injury.
出处 《中国小儿急救医学》 CAS 2008年第4期345-347,共3页 Chinese Pediatric Emergency Medicine
基金 国家自然科学基金资助项目(30770944) 国家自然科学基金资助项目(30672261)
关键词 高氧 早产 硫氧还蛋白 肺损伤 Hyperoxia Premature Thioredoxin Lung injury
  • 相关文献

参考文献9

  • 1钱莉玲,常立文,张谦慎,容志惠.85%高浓度氧长期暴露诱发早产大鼠肺损伤(英文)[J].中国当代儿科杂志,2003,5(2):95-99. 被引量:21
  • 2Yalcin A. Quantification of thioredoxin mRNA expression in the rat hippocampus by real-time PCR following oxidative stress, Acta Biochim Pol, 2004, 51 (4) : 1059-1065.
  • 3袁祖贻,刘艳,岸本千晴,盐路圭介,淀井淳司,刘治全.特莫普利上调心肌硫氧化还原蛋白表达减轻心肌炎[J].中华内科杂志,2003,42(5):309-312. 被引量:4
  • 4Okuyama H, Shimahara Y, Nakamura H, et al. Thioredoxin prevents thioacetamide-induced acute hepatitis. Comp Hepato, 2004, 3(Suppl 1) :S6.
  • 5Jakkula M, Le Cras TD, Gebb S, et al. Inhibition of angiogenesis decreases alveolarization in the developing rat lung. Am J Physiol Lung Cell Mol Physiol, 2000, 279 (3) : L600-607.
  • 6Koe A, Mathews CK, Wheeler LJ, et al. Thioredoxin is required for deoxyribonueleotide pool maintenance during S phase. J Biol Chem, 2006, 281 (22) : 15058-15063.
  • 7Andoh T, Chock PB, Chiueh CC. The roles of thioredoxin in protection against oxidative stress-induced apoptosis in SH-SY5Y cells. J Biol Chem, 2002, 277(12):9655-9660.
  • 8Tanaka T, Hosoi F, Yamaguchi IW, et al. Thioredor3n-2 (TRX-2) is an essential gene regulating mitochondria-dependeat apoptosis. EMBO J, 2002, 21(7) : 1695-1703.
  • 9Yegorova S, Yegorov O, Lou MF. Thioredoxin induced antioxidant gene expressions in human lens epithelial cells. Exp Eye Res, 2006, 83 (4) : 783-792.

二级参考文献18

  • 1[7]Jobe AJ. The new BPD: an arrest of lung development [J]. Pediatr Res, 1999, 46(6): 641-643.
  • 2[8]Jobe AH, Ikegami M. Prevention of bronchopulmonary dysplasia [J]. Curr Opin Pediatr, 2001, 13(2): 124-129.
  • 3[1]Saugstad OD. Bronchopulmonary dysplasia and oxidative stress: are we closer to an understanding of the pathogenesis of BPD? [J]. Acta Paediatr, 1997, 86(12): 1277-1282.
  • 4[2]Jakkula M, Le Cras TD, Gebb S, et al. Inhibition of angiogenesis decreases alveolarization in the developing rat lung [J]. Am J Physiol Lung Cell Mol Physiol, 2000, 279(3): L600-607.
  • 5[3]Yam J, Frank L, Roberts RJ. Oxygen toxicity: comparison of lung biochemical responses in neonatal and adult rats [J]. Pediatr Res, 1978, 12(2): 115-119.
  • 6[4]Coalson JJ, Kuehl TJ, Prihoda TJ, et al. Diffuse alveolar damage in the evolution of bronchopulmonary dysplasia in the baboon [J]. Pediatr Res, 1988, 24(3): 357-366.
  • 7[5]Crapo JD, Peters-Golden M, Marsh-Salin J, et al. Pathologic changes in the lungs of oxygen-adapted rats: a morphometric analysis [J]. Lab Invest, 1978, 39(6): 640-653.
  • 8[6]Thet LA, Wrobel DJ, Crapo JD, et al. Morphologic aspects of the protection by endotoxin against acute and chronic oxygen-induced lung injury in adult rats [J]. Lab Invest, 1983, 48(4): 448-457.
  • 9Kodama M, Matsumoto Y, Fujiwara M, et al. A novel experimental model of giant cell myocarditis induced in rats by immunnization with cardiac myosin fraction. Clin Immunol Immunopathol, 1990,57:250-262.
  • 10Kaneko M, Masuda H, Suzuki H, et al. Modification of contractile proteins by oxygen free radicals in rat heart. Mol Cell Biochem,1993,125 : 163-169.

共引文献23

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