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核因子κB在大鼠双侧后肢缺血再灌注致肺损伤中的表达及意义 被引量:3

Expression and significance of nuclear factor κB in lun g injury after ischemia/reperfusion in hind limbs of rats
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摘要 目的 :探讨核因子κB(NF κB)在大鼠双侧后肢缺血再灌注 (I/R )致肺损伤中的表达及意义。方法 :建立大鼠双侧后肢I/R模型 :48只大鼠随机分为假手术组 (Ⅰ组 ,n =8)、缺血组 (Ⅱ组 ,n =8)、缺血再灌注组 (Ⅲ组 ,n =3 2 )。Ⅱ组在缺血 4h末 ,Ⅲ组分别于再灌注 4,12 ,2 4,48h切取双肺 ,应用半定量RT PCR和Westernblot方法检测肺组织NF κBp65/IκBβ的mRNA和蛋白产物表达。结果 :Ⅲ组各时点NF κBp65mRNA表达较Ⅰ、Ⅱ组增加 ,再灌注后 12h达高峰。p65蛋白产物表达亦逐渐增加 ,12h达高峰 ,持续到术后 48h ;IκBβ的mRNA和蛋白表达在I/R后同样开始增加 ,2 4h的表达量最多。结论 :NF Objective: To investigate the effect of sk el etal muscle ischemia/reperfusion on the expression of nuclear factor kappa B(NF -κB) in lung injury of rats. Methods: Rat models of hind lim bs ischemia/reperfusion were established. Forty-eight rats were divided into 3groups: sham operation group(groupⅠ, n=8), ischemia group(groupⅡ, n=8),ischemia/reperfusion injury group(groupⅢ, n=32), which included subgroup s of 4, 12, 24, 48 hours after reperfusion. The changes of mRNA and protein expr ession of NF-κB p65/ IκBβ in lung were determined by using RT-PCR or Wester n blot. Results: In group Ⅲ, NF-κB p65 mRNA increased quick ly after reperfusion and reached peak 12 hours after reperfusion. The p65 detect ed by using Western blot reached peak 12 hours after reperfusion and then decrea sed slowly, but still remained at high level 48 hours after reperfusion. Express ion of IκBβ mRNA and protein in lung also increased after reperfusion and reac hed peak 24 hours after reperfusion. Conclusion: The NF-κBp6 5/IκBβ may play an important role in the damage of lung function after skeleta l muscle ischemia/reperfusion injury in rats.
出处 《中国医科大学学报》 CAS CSCD 北大核心 2004年第1期9-11,共3页 Journal of China Medical University
基金 国家自然科学基金资助项目 ( 30 371 40 1 )
关键词 核因子ΚB 缺血再灌注 肺损伤 nuclear factor kappa B ischemia/reperfusion in jury lung injury
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  • 1[1]Tassiopoulos AK, Carlin RE, Gao Y, et al. Role of nitric oxide and tumor necrosis factor on lung injury caused by ischemia/reperfusion of the lower extremities[J]. J Vasc Surg,1997, 26(4): 647-656.
  • 2[2]Kyriakides C, Austen W, Wang Y, et al. Skeletal muscle reperfusion injury is mediated by neutrophils and the complement membrane attack complex[J]. Am J Physiol,1999, 277(6): C1263-C1268.
  • 3[3]Anderson BO, Brown JM, Harken AH. Mechanisms of neutrophilmediated tissue injury[J]. J Surg Res, 1991, 51(2): 170-179.
  • 4[4]Barry MC, Kelly CJ, Abdih H, et al. Differential effects of lower limb revascularisation on organ injury and the role of the amino acid taurine[J]. Eur J Vasc Endovasc Surg, 1997, 13(2): 193-201.
  • 5[5]Paterson IS, Klausner JM, Pugatch R, et al. Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery[J]. Ann Surg, 1989, 209(2): 231-236.
  • 6[6]Gaines GC, Welborn MB III, Moldawer LL, et al. Attenuation of skeletal muscle ischemia/ reperfusion injury by inhibition of tumor necrosis factor[J]. J Vasc Surg, 1999, 29(2): 370-376.
  • 7[7]Collins T, Read MA, Neish AS, et al.. Transcriptional regulation of endothelial cell adhesion molecules: NF-kappa B and cytokine-inducible enhancers[J]. FASEB J, 1995, 9(10): 899-909.
  • 8[8]Ross SD, Kron IL, Gangemi JJ, et al. Attenuation of lung reperfusion injury after transplantation using an inhibitor of nuclear factor-κB[J]. Am J Physiol Lung Cell Mol Physiol, 2000, 279(3): L528-L536.

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