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肿瘤坏死因子相关蛋白9抑制核因子κB核转位对巨噬细胞炎症因子表达的影响 被引量:6

C1q/ tumor necrosis factor-related protein 9 decreases pro-inflammatory cytokines expression in macrophage cells by inhibiting nuclear factor-κB translocation
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摘要 目的 探究肿瘤坏死因子相关蛋白9(CTRP9)对氧化型低密度脂蛋白(ox-LDL)诱导RAW 264.7小鼠巨噬细胞抗炎作用和机制. 方法 选择RAW264.7小鼠巨噬细胞系,分为对照组(对照组)、oxLDL组、gCTRP9+ oxLDL组.采用油红O染色鉴定泡沫细胞,免疫印迹分析检测肿瘤坏死因子(TNF)-α、单核细胞趋化蛋白(MCP-1)及胞浆、细胞核核转录因子κB (NF-κB) p65蛋白表达水平. 结果 与对照组比较,ox-LDL组巨噬泡沫细胞中MCP-1蛋白和TNF-α蛋白表达上调(P<0.05),与ox-LDL组比较,gCTRP9+ oxLDL组TNF-α和MCP-1的蛋白表达降低(P<0.05).oxLDL组与对照组比较,NF-κB表达增加(P<0.05);与ox-LDL组比较,gCTRP9组2h和8hNFκB P65表达下降,1.03±0.06比0.17±0.10和0.31±0.03(均P<0.05). 结论 oxLDL可诱导巨噬细胞表达TNF-α和MCP-1,gCTRP9可减少oxLDL的促炎作用,NF-κB信号转导通路可能参与了上述抗炎作用机制,提示gCTRP9可能具有抗炎,抗动脉粥样硬化的保护性作用. Objective To investigate the anti-inflammatory effect of C1q/ tumor necrosis factor (TNF)-related protein 9 (CTRP9) in RAW264.7 mouse macrophage cells treated with oxidized low density lipoprotein (oxLDL),and to explore its mechanism.Methods RAW264.7 mouse macrophage cells were divided into three groups:the control group,the oxLDL group (treated with oxLDl) and the gCTRP9-oxLDL group (pretreated with recombinant globular domain of CTRP9 and stimulated by oxLDL).Foam cells were detected by oil red O staining.Western blot was used to detect the expressions of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein 1 (MCP-1).In addition,the expression levels of NF-κB p65 in cytoplasm and nucleus proteins extraction were both determined.Results The relative levels of MCP-1 and NF-κB were increased in the oxLDL group as compared with the control group (1.66±0.09 vs.1.03±0.10,0.52±0.11 vs.1.03±0.06,both P〈0.05).The expression levels of TNF-α and MCP-1 were decreased in gCTRP9+oxLDL group as compared with the oxLDL group (both P〈0.05).The expression level of NF κB p65 in nucleus 2 and 8 h after treatment was lower in the gCTRP9+oxLDL group than in the oxLDL group (1.03±0.06 vs.0.17±0.10,0.31±0.03,both P〈0.05).Conclusions oxLDL may induce the expressions of inflammatory cytokines of TNF α and MCP-1 in macrophage ceils.gCTRP9 pretreatment could reduce the oxLDL-induced pro inflammatory effect and nuclear factor κB translocation may be involved in this process,which suggests that gCTRP9 may play a protective role in anti inflammatory and anti-atherosclerosis.
出处 《中华老年医学杂志》 CAS CSCD 北大核心 2015年第6期664-666,共3页 Chinese Journal of Geriatrics
基金 国家自然科学基金(NSFC:81350025)
关键词 肿瘤坏死因子 动脉粥样硬化 Tumor necrosis factor Atherosclerosis
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参考文献10

  • 1Hansson GK, Hermansson A. The immune system in atherosclerosis[J]. Nat Immunol, 2011. 12: 20.'1-212.
  • 2Intimal R, Dcalactti A, Galkina E, et al. I.eukocyte influx in atheroselerosis [J] . Curr Drug Targets, 2007, 8: 1239-1248.
  • 3Moore K J, Tabas I. Macrophages in the pathogenesis of atherosclerosis[J]. Cell, 2011, 145; 341 355.
  • 4李明春,陆林,陈秋静,张瑞岩,张奇,沈卫峰.血清CTRP9水平与冠心病的关系[J].国际心血管病杂志,2013,40(5):323-325. 被引量:10
  • 5刘天骄,郭媛,李婷婷,张建宁,李俊,张鹏.血清CTRP9、APN水平与急性冠脉综合征的相关性[J].山东大学学报(医学版),2014,52(9):58-62. 被引量:8
  • 6ZhengQ, Yuan Y, Yi W. et al. Clq/TNF related proteins, a family of novel adipokines, induce vascular relaxation through the adiponectin receptor 1/AMPK/eN()S/nitric oxide signaling pathway[J]. Arterioscler Thromh Vasc Biol, 2011, 31 : 2616-2623.
  • 7mmra Y. Shibata R, ()hashi K, et al. Adipose- derived factor CTRP9 attenuates vascular smooth muscle cell proliferation and neointimal formation[J3. FASEB J. 2013, 27:25 33.
  • 8Ionizzi G, Karin M. The two NF-kappaB activation pathways and their role in innate and adaptive immunity[J] Trends Inmmnol, 2004, 25: 280-288.
  • 9Pnkenburg (). Platz J, Beisswenger C, et al. Inhibition of NF kappaB mediated inflammation by siRNA expressed by recombinant adeno-associated virus[J]. J Virol Methods, 2004. 12: 119-122.
  • 10Yao R. Cheng X, Ghen Y, et al. Molecular mechanisms of irbesartan suppressing atherosclerosis in high cholesterol diet apolipoprotein E knock-out mice[J]. Int J Cardiol, 2010, 139:113 122.

二级参考文献29

  • 1Wong GW, Wang J, Hug C, et al. A family of Acrp30/ adiponectin structural and functional paralogs[J]. Proc Natl Acad Sci U S A,2004,101(28) :10302- 10307.
  • 2Scherer PE, Williams S, Fogliano M, et al. A novel serum protein similar to CIq, produced exclusively in adipocytes [J]. J Biol Chem,1995,270(45) :26746-26749.
  • 3Sehfiffler A, Buechler C. CTRP family: linking immunity to metabolism[J]. Trends Endocrinol Metab, 2012, 23 (4): 194-204.
  • 4Wong GW, Krawczyk SA, Kitidis-Mitrokostas C, et al. Identification and characterization of CTRP9, a novel secreted glycoprotein, from adipose tissue that reduces serum glucose in mice and forms heterotrimers with adiponectin[J]. FASEB J, 2009, 23(1): 241-258.
  • 5Kambara T, Ohashi K, Shibata R, et al. CTRP9 protects against myocardial injury following isehemia-reperfusion through AMPK-dependent mechanism [J]. J Biol Chem, 2012, 287(23) : 18965-18973.
  • 6Su H, Yuan Y, Wang XM,et al. Inhibition of CTRP 9, a novel and cardiac-abundantly expressed cell survival molecule by TNF-alpha-initiated oxidative signaling contributes to exacerbated cardiac injury in diabetic mice [J]. Basic Res Cardiol, 2013, 108(1): 315.
  • 7Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction): developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons; endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine [J]. Circulation, 2007 ,116(7):e148-e304.
  • 8Antman EM, Hand M, Armstrong PW, et al. 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee [J]. Circulation, 2008,117 (2) :296-329.
  • 9Fruebis, J, Tsao, "IS, Javorschi, S, et al. Proteolytic cleavage product of 30-kDa adipocyte complement-related protein increases fatty acid oxidation in muscle and causes weight loss inmiee[J]. Proc Natl Acad Sci U S A, 2001, 98 (4): 2005-2010.
  • 10Berg AH, Combs TP, Du X, et ah The adipocyte-secreted protein Acrp30 enhances hepatic insulin action[J]. Nat Med, 2001,7(8) :947-953.

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