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补体Clq对Aβ纤维诱导的小胶质细胞炎性反应的影响 被引量:2

Influence of complement Clq on beta amyloid fibers-induced BV-2 microglia inflammation
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摘要 目的探讨补体Clq对Aβ纤维诱导的小胶质细胞炎性反应的影响。方法在一定浓度Aβ纤维刺激的基础上,向BV-2小胶质细胞中加入不同浓度Clq,并且利用C1qA竞争性与Ap的结合以完成对比实验,利用夹心酶联免疫吸附法(ELISA)测定上清液及细胞裂解液中白介素(IL)-6和肿瘤坏死因子(TNF)-α的浓度。结果在AB纤维刺激下,加入50nmol/L补体Clq后,上清液TNF-α浓度较单独加入Aβ纤维明显增加(F=1177.270,P〈0.05);但在此基础上加入补体ClqA后,TNF-α浓度降低(P〈0.05)。除阳性对照组外,各实验组上清液及细胞裂解液中IL-6浓度相互比较差异无统计学意义(均P〉0.05)。结论补体Clq可能通过促炎性因子TNF-α增强了Aα诱导的BV-2小胶质细胞的炎性反应。 Objective The impact of complement Clq on inflammation in beta amyloid- stimulated microglia. Methods After the cultured BV-2 microglial cells were treated with 100 mg/L betaamyloid fibers (fAβs), some of them were given Clq, others were given Clq and ClqA. Then, interleukin-6 (IL-6) and tumor necrosis factor a (TNF-α) in the supernatant and cell lysate were determined by the sandwich ELISA. Results A significant increase in TNF-α started at giving 50 nmol/L Clq after 100 mg/L fAβs(F= 1177.27, P〈0.05), while the release of TNF-α was significantly suppressed by using 50 nmol/L ClqA on basis of this(P〈0.05). The level of IL-6 showed no above change. Conclusions Clq may enhance the inflammation of Aβ-induced BV-2 microglia cells and TNF-α may play important role in this effect.
出处 《中华老年医学杂志》 CAS CSCD 北大核心 2013年第1期96-98,共3页 Chinese Journal of Geriatrics
基金 广东省医学科学基金(C2009031) 广州市科技计划项目(2010Y1-C101)
关键词 阿尔茨海默病 补体C1Q 淀粉样Β蛋白前体 小神经胶质细胞 Alzheimer disease Complement Clq Amyloid beta-peptides Microglia
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参考文献9

  • 1Hashioka S, Monji A, Ueda T, et al. Amyloid-beta fibril formation is not necessarily required for microglial activation by the peptides. Neurochem Int, 2005,47 : 369-376.
  • 2Sjoberg AP, Trouw LA, Blom AM. Complement activation and inhibition: a delicate balance. Trends Immunol, 2009,30:83-90.
  • 3Strohmeyer R, Ramirez M, Cole GJ, et al. Association of factor H of the alternative pathway of complement with agrin and complement receptor 3 in the Alzheimer's disease brain. J Neuroimmunol, 2002, 131: 135-146.
  • 4罗晓光,王燕,葛春林,任艳,禹红梅,王秋爽,董理,张朝东.阿尔茨海默病中C1q诱导氧化神经毒性研究[J].中国神经免疫学和神经病学杂志,2008,15(4):252-254. 被引量:5
  • 5Pisalyaput K, Tenner AJ. Complement component Clq inhibits beta-amyloid- and serum amyloid P- induced neurotoxicity via caspase- and calpain- independent mechanisms. J Neurochem, 2008, 104: 696-707.
  • 6Fraser DA, Pisalyaput K, Tenner AJ. Clq enhances microglial clearance of apoptotic neurons and neuronal blebs and modulates subsequent inflammatory cytokine production. J Neurochem, 2010, 112: 733- 743.
  • 7Benoit ME, Tenner AJ. Complement protein Clq- mediated neuroprotection is correlated with regulation of neuronal gene and microRNA expression. J Neurosci, 2011, 31:3459-3469.
  • 8Ouerfurth HW, LaFerla FM. Alzheimer's disease. N Engl J Med, 2010, 362: 329-344.
  • 9李玮,索爱琴,张杰文,赵建华,葛继晖,秦得营,贺显军,姜晓峰.β淀粉样蛋白对原代小胶质细胞炎性作用机制的研究[J].中华老年医学杂志,2011,30(6):516-518. 被引量:1

二级参考文献21

  • 1Zhu X,Rottkamp CA,Boux H,et al.Activation of p38 kinase Links tau phosphorylation,oxidative stress,and cell cycle-related events in Alzheimer disease.J Neuropathol Exp Neurol,2000,59:880-888.
  • 2Sun J,Li M,Han J,et al.Sensitization of differentiated PC12 Cells to apoptosis by presenilin-2 is mediated by p38.Biochem Biophys Res Commun,2001,287:536-541.
  • 3Hitti E,Iakovleva T,Brook M,et al.Mitogen-activated protein kinase-activated protein kinase 2 regulates tumor necrosis factor mRNA stability and translation mainly by altering tristetraprolin expression,stability,and binding to adenine/uridine-rich element.Mol Cell Biol,2006,26:2399-2407.
  • 4Lukas SM,Kroe RR,Wildeson J,et al.Catalysis and function of the p38 alpha.MK2a signaling complex.Biochemistry,2004,43:9950-9960.
  • 5Tichler A K,Wade JD,Separovic F.The role of Abeta peptides in Alzheimer′s disease.Protein Pept Lett,2005,12:513-519.
  • 6Griffin WS,Sheng JG,Royston MC,et al.Glial-neuronal interactions in Alzheimer′s disease:the potential role of a `citokine cycle` in disease progression.Brain Pathol,1998,8:65-72.
  • 7Eikelenboom P,van Exel E,Hoozemans JJ,et al.Neuroinflammation-an early event in both the history and pathogenesis of Alzheimer′s disease.Neurodegener Dis,2010,7:38-41.
  • 8Lorton D.β-Amyloid protein induce inereased release of in-terlekin-1β from lipopolysaccharids-activated human-monocyts.J Neuroimmunol,1996,67:21-29.
  • 9Kotlyarov A,Neininger A,Schubert C,et al.MAPKAP kinase 2 is essential for LPS-induced TNF-alpha biosynthesis.Nat Cell Biol,1999,1:94-97.
  • 10Culbert AA,Skaper SD,Howlett DR,et al.MAPK activated protein kinase 2 deficiency in microglia inhibits proinflammatory mediator release and resultant neurotoxicity.Relevance to neuroinflammation in a transgenic mouse model of Alzheimer disease.J Biol Chem,2006,281:23658-23667.

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  • 1Gholamreza Azizi,Abbas Mirshafiey.The potential role of proinflammatory and antiinflammatory cytokines in Alzheimer disease pathogenesis[J].Immunopharmacology and Immunotoxicology.2012(6)
  • 2Kazuo Washida,Masafumi Ihara,Keiko Nishio,Youshi Fujita,Takakuni Maki,Mahito Yamada,Jun Takahashi,Xiaofeng Wu,Takeshi Kihara,Hidefumi Ito,Hidekazu Tomimoto,Ryosuke Takahashi.Nonhypotensive Dose of Telmisartan Attenuates Cognitive Impairment Partially Due to Peroxisome Proliferator-Activated Receptor-γ Activation in Mice With Chronic Cerebral Hypoperfusion[J].Stroke.2010(8)
  • 3McAfoose J, Baune BT. Evidence for cytokine model of cognitive function [J]. Neurosci Biobehav Rev, 2009, 33:355 -366.
  • 4Zou CG, Zhao YS, Gao SY, et al. Homocysteine promotes proliferation and activation of microglia[J]. Neurobiol Aging, 2010, 31:2069-2079.
  • 5Sharma B, Singh N. Salutary effect of NF -kB inhibitor and folacin in hyperhomocysteinemia hyperlipidemia induced vascular dementia[J]. Prog Neuropsychopharmacol Biol Psychiatry, 2012, 38: 207 -215.
  • 6Wu S, Gao X, Yang S, et al. Protective Effects of Cariporide on Endothelial Dysfunction Induced by Homocysteine[J]. Pharmacology, 2013, 92: 303- 309.
  • 7JinWJ, Feng SW, Feng Z, et al. Minocycline improves postoperative cognitive impairment in aged mice by inhibiting astrocytic activation [J]. Neuroreport, 2014, 25:1- 6.
  • 8WeismanD, Hakimian E, Ho GJ. Interleukins, inflammation, and mechanisms of Alzheimer's disease [J]. Vitam Horm, 2006, 74:505 -530.
  • 9Lin HC, Song TY, Hu ML. S-adenosylhomocysteine promotes the invasion of C6 glioma cells via increased secretion of matrix metalloproteinase 2 in murine microglial BV2 cells[J].ToxicolSci, 2009, 112:322 -330.
  • 10邬烈铭,朱文芳,裴瑜,瞿正万,童捷,张婷婷,王勇,朱莉娜,金莹,王豪,闵婕,王强,倪培华.老年性痴呆患者认知功能与血清炎性细胞因子浓度的相关研究[J].中华临床医师杂志(电子版),2012,6(11):105-108. 被引量:21

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