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肺角质细胞生长因子受体在大鼠急性脊髓损伤后肺水肿中的表达及作用 被引量:2

Expression of lung keratinocyte growth factor receptor in the pulmonary edema of rats with acutespinal cord injury
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摘要 目的探讨大鼠急性脊髓损伤(acute spinal cord injury,ASCI)后不同时相点肺组织角质细胞生长因子受体(keratinocyte growth factor receptor,KGFR)的表达及其与肺水肿的关系。方法成年Wistar大鼠32只,体重240-260g,雌雄不限。按随机数字表法分为实验组和对照组,每组16只,每组分为造模后24h、3d、1周、2周共4个时相点,每个时相点4只大鼠。实验组均采用C。脊髓Allen打击法制作大鼠ASCI模型,打击剂量为10g×2.5cm,对照组仅暴露c,脊髓。检测各时相点两组大鼠肺湿干重比,使用Westernblot技术检测肺组织KGFR蛋白表达水平,RT-qPCR技术检测肺组织KGFRmRNA表达水平。结果大鼠ASCI后肺组织KGFR蛋白及mRNA表达水平均于伤后24h开始下降,分别为0.23±0.06,0.0121±0.0023,伤后3d达最低值,分别为0.17±0.04,0.0085±0.0017,伤后1周含量开始回升。伤后24h和3d实验组肺组织KGFRmRNA表达与对照组差异有统计学意义(P〈0.05),伤后各时相点KGFR蛋白表达均与对照组差异有统计学意义(P〈0.05)。KGFR表达的变化趋势与肺水肿严重程度的变化趋势同步。结论ASCI后肺组织KGFR表达显著降低,可能与ASCI后肺水肿的形成有关。 Objective To investigate the expression of lung keratinocyte growth iactor receptor (KGFR) in rats with acute spinal cord injury (ASCI) in different time points and its role in lung edema. Methods Thirty-two adult Wistar rats weighing 240 g to 260 g were assigned to experimental group ( n = 16) and control group (n = 16) according to the random number table. Each group consisted of time points of 24 hours, 3 days, 1 week and 2 weeks after the modeling (4 rats per time point). A rat model of ASCI in experimental group was induced at C7 segment by dropping a weight of 10 g from the height of 2.5 cm ( Allen' s method). In control group, laminas were removed only, leaving spinal cord at C7 intact. Rats were sacrificed at each time point for measurement of lung wet/dry weight ratio, Western blot analysis of expression of lung KGFR protein and RT-qPCR detection of lung KGFR mRNA expression. Results After ASCI in rats, the expressions of lung KGFR protein and mRNA began to drop at 24 hours (0.23 ±0.06, 0,012 1 ±0.002 3), reached the trough at 3 days (0.17 ±0.04, 0.008 5±0.001 7) and picked up at 1 week. Expression of lung KGFR mRNA in experiment group showed statistically significant difference from that in control group at 24 hours and 3 days ( P 〈 0.05 ) , whereas in each time point the difference of KGFR protein expression between experiment and control groups was statistically significant(P 〈0.05 ) . Variation trend of KGFR expression was in parallel with the severity degree of pulmonary edema. Conclusion Lung KGFR presents significant down-regulation in ASCI rats and this may be associated with the development of pulmonary edema after ASCI.
出处 《中华创伤杂志》 CAS CSCD 北大核心 2013年第10期996-999,共4页 Chinese Journal of Trauma
基金 上海市教育委员会科研创新重点资助项目(12ZZ079) 上海市科学技术委员会自然科学基金资助项目(11ZRl448400)
关键词 脊髓损伤 肺水肿 角质细胞生长因子受体 Spinal cord injurer Pulmonary edema Keratinocyte growth factor receptor
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参考文献14

  • 1南国新,廖维宏,伍亚民,王莉,王旭.大鼠急性脊髓损伤后肺组织的病理改变及其意义[J].中国脊柱脊髓杂志,2007,17(3):214-217. 被引量:9
  • 2Veeravagu A, Jiang B, Rincon F, et al. Acute respiratory dis- tress syndrome and acute lung injury in patients with vertebral column fracture(s) and spinal cord injury: a nationwide inpatient sample study. Spinal Cord, 2013, 51 (6) :461 -465.
  • 3Aarabi B, Harrop JS, Tator CH, et al. Predictors of pulmonary complications in blunt traumatic spinal cord injury. J Neurosurg Spine, 2012, 17 (1 Suppl 1) :38 -45.
  • 4迟大明,朱悦.颈髓损伤后气管切开相关因素分析[J].中华创伤杂志,2005,21(12):899-902. 被引量:19
  • 5Chandel NS, Budinger GR, Mutlu GM, et al. Keratinocyte growth factor expression is suppressed in early acute lung injury/acute re- spiratory distress syndrome by smad and c - Abl pathways. Crit Care Med, 2009, 37(5):1678-1684.
  • 6Yong T, Lili Y, Wen Y, et al. Pulmonary edema and hemor- rhage, possible causes of pulmonary infection and respiratory fail- ure in the early stage of lower spinal cord injury. Med Hypothe- ses, 2012, 79(3):299-301.
  • 7Gris D, Hamilton EF, Weaver LC. The systemic inflammatory re- sponse after spinal cord injury damages lungs and kidneys, Exp Neurol, 2008, 211 ( 1 ) :259 - 270.
  • 8Leal Filho MB, Morandin RC, de AImeida AR, et al. Hemody- namic parameters and neurogenic pulmonary edema following spi- nal cord injury: an experimental model Arq Neumpsiquiatr, 2005, 63(4) :990 -996.
  • 9BorokZ, DantoSI, DimenLL, et al. Na(+) -K(+) -AT- Pase expression in alveolar epithelial cells : upregulation of active ion transport by KGF. Am J Physiol, 1998, 274 ( 1 Pt 1 ) : L149 - L158.
  • 10Devivo MJ. Epidemiology of traumatic spinal cord injury: trends and future implications. Spinal Cord, 2012, 50(5 ) :365 -372.

二级参考文献30

  • 1刘荫秋,安波,李曙光,赖西南,王建民.高速高能战创伤间接伤的特点及其致伤机理[J].中华创伤杂志,1995,11(1):22-24. 被引量:34
  • 2南国新,廖维宏,伍亚民,王莉,王旭.大鼠急性脊髓损伤后肺组织的病理改变及其意义[J].中国脊柱脊髓杂志,2007,17(3):214-217. 被引量:9
  • 3Wrathall JR,Pettegrew RK,Harvey F. Spinal cord contusion in the rat :production of graded,reproducible,injury groups[Jl.Exp Neurol, 1985,88 ( 1 ) : 108-122.
  • 4DeVivo MJ,Black KJ,Stover SL. Causes of death during the first 12 years after spinal cord injury [J].Arch Phys Med Re- habil, 1993,74(3) :248-254.
  • 5Jackson AB,Groomes TE.Incidence of respiratory complications following spinal cord injury [J].Arch Phys Med Rehabil,1994, 75 ( 3 ) : 270-275.
  • 6Hegde A,Zhang H,Moochhala SM,et al.Neurokinin-I receptor antagonist treatment protects mice against lung injury in polymicrobial sepsis[J].J Leukoc Biol,2007,82(3):678-685.
  • 7Bhatia M,Slavin J,Cao Y',et al.Preprotachykinin-A gene dele- tion protects mice against acute panereatitis and associated lung injury[J].Am J Physiol,2003,284:G830-G836.
  • 8Lau HY,Wong FL,Bhatia M. A key role of neurokinin 1 re- ceptors in acute pancreatitis and associated lung injury lJI. Biochem Biophys Res Commun, 2005,327 (2) : 509-515.
  • 9Ng SW,Zhang H,Hegde A,et al. Role of preprotachykinin-A gene products on multiple organ injury in LPS-induced endo- toxemia[J].J Leukoc Biol, 2008,83 (2) : 288-295.
  • 10Sio SW,Moochhala S,Lu J,et al.Early protection fi'om burn- induced acute lung injury by deletion of preprotachykinin-A gene[J].Am J Respir Care Med,2010,181 (1) :36-46.

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