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PPARγ和NF-κB在肺纤维化中的表达与意义 被引量:6

Expression and role of peroxisome proliferator-activated receptor γ and nuclear factor-κB in pulmonary fibrosis
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摘要 目的:观察过氧化物酶体增殖物激活受体γ(PPARγ)和核因子-κB(NF-κB)在肺纤维化患者肺组织中的表达情况,探讨其在肺纤维化发病中的作用。方法:采用免疫组织化学方法检测16例肺纤维化患者与10例正常对照肺组织标本中PPARγ、NF-κB的表达情况。结果:肺纤维化组PPARγ的阳性表达记数为0.35±0.08,低于正常对照组的0.42±0.04(P<0.05)。肺纤维化组NF-κB的阳性表达记数为0.51±0.11,高于正常对照组的0.38±0.04(P<0.05)。肺纤维化组的PPARγ和NF-κB的表达呈负相关(P<0.05)。结论:肺组织中PPARγ的表达减弱、NF-κB的表达增强在肺纤维化的发病过程中起作用,为临床治疗肺纤维化提供了新思路。 Objective: To evaluate the expression of peroxisome proliferator-activated receptor γ (PPARγ) and nuclear factor-kB (NF-kB) in lungs in patients with pulmonary fibrosis, and to explore their effect on the pathogenesis of pulmonary fibrosis. Methods: Immunohistochemical technology was performed to investigate the PPARγand NF-kB expression in lung specimens from 16 cases of pulmonary fibrosis and 10 cases of normal controls. Results: The positive score of PPAR3, (0. 35 ± 0. 08 ) in fibrosis group was lower than that in control group (0. 42 ± 0.04, P 〈 0. 05). The positive score of NF-kB (0. 51 ±0. 11 ) in fibrosis group was higher than that in control group (0. 38 ±0. 04, P 〈0. 05). There was negative correlation between PPARγ and NF-kB expression in fibrosis group ( P 〈 0. 05 ). Conclusion: The decreased expression of PPARγ and enhanced expression of NF-kB play a role in the pathogenesis of pulmonary fibrosis, which may provide a new idea for treating this disease.
出处 《北京大学学报(医学版)》 CAS CSCD 北大核心 2009年第5期545-547,共3页 Journal of Peking University:Health Sciences
关键词 肺纤维化 PPARΓ NF-ΚB Pulmonary fibrosis PPAR gamma NF-kappa B
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参考文献10

  • 1Berger J, Moller DE. The mechanisms of action of PPARs [J]. Annu Rev Ned, 2002, 53:409 -435.
  • 2Tergaonkar V. NFkappaB pathway: a good signaling paradigm and therapeutic target [J]. Int J Biochem Cell Biol, 2006, 38(10) : 1647 - 1653.
  • 3Wang K, Wan YJ. Nuclear receptors and inflammatory diseases [J]. Exp Biol Med (Maywood), 2008, 233(5): 496-506.
  • 4Fogo AB. Potential for peroxisome proliferator-activated receptorgamma agonists in progression: beyond metabolism [ J ]. Curr Opin Nephrol Hypertens, 2008, 17 (3) : 282 - 285.
  • 5Yang L, Chan CC, Kwon OS, et al. Regulation of peroxisome proliferator-activated receptor-gamma in liver fibrosis [ J]. Am J Physiol Gastrointest Liver Physiol, 2006, 291 (5) : G902 -911.
  • 6Henderson BC, Sen U, Reynolds C, et al. Reversal of systemic hypertension-associated cardiac remodeling in chronic pressure overload myocardium by ciglitazone [ J]. Int J Biol Sci, 2007, 3 (6) : 385 -392.
  • 7Belvisi MG, Hele DJ. Peroxisome proliferator-activated receptors as novel targets in lung disease [ J]. Chest, 2008, 134 ( 1 ) : 152 - 157.
  • 8Milam JE, Keshamouni VG, Phan SH, et al. PPAR-gamma agonists inhibit profibrotic phenotypes in human lung fibroblasts and bleomycin-induced pulmonary fibrosis [ J]. Am J Physiol Lung Cell Mol Physiol, 2008, 294(5) : L891 -901.
  • 9于红.核转录因子NF-κB与肺纤维化[J].中国实用内科杂志,2006,26(8):1203-1204. 被引量:6
  • 10De Bosscher K, Vanden Berghe W, Haegeman G. Cross-talk between nuclear receptors and nuclear factor kappaB [ J]. Oncogene, 2006, 25(51): 6868-6886.

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