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载脂蛋白E基因敲除小鼠脑部TNF-α和IL-1β及IL-8的水平升高 被引量:2

Apo E gene knockout causes high expressions of TNF-α,IL-1β and IL-8 in mouse brain
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摘要 目的探讨载脂蛋白E基因敲除(Apo E-/-)后小鼠脑部海马区和皮质区肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)及IL-8表达变化。方法 4周龄野生型和Apo E-/-雄性小鼠各10只,饲养12周后断颈处死。采集血液样本进行血脂水平检测;将脑组织固定后切片,HE染色观察形态学改变;免疫组织化学染色检测TNF-α、IL-1β、IL-8蛋白表达。结果IL-1β和IL-8在Apo E-/-小鼠海马区和皮质区表达的阳性细胞数均显著高于野生型小鼠。TNF-α在Apo E-/-小鼠皮质区表达的阳性细胞数显著高于野生型小鼠,Apo E-/-小鼠海马区TNF-α的表达强度高于野生型小鼠。结论 Apo E-/-小鼠脑部TNF-α、IL-1β、IL-8表达增加。 Objective To investigate the expression profile of tumor necrosis factor α (TNF-α), intedeukin 1β (IL-1β) and IL-8 in the hippocampus and cerebral cortex of apolipoprotein E (ApoE) knockout (ApoE-/- ) mice. Methods Twenty 4-week-old male mice were divided into 2 groups: wild-type mice and ApoE-/- mice, 10 mice for each. After 12-week feeding, the blood sample was taken for serum lipid test and brain tissue were obtained for fixation and embedding. The histological changes of the hippocampus and cerebral cordex were observed by HE staining and the expressions of TNF-α, IL-1β and IL-8 proteins were detected by immunohistochemistry. Results Compared with the wild-type mice, the numbers of the IL-115 and IL-8-positive cells were markedly elevated in the hippocampus and cerebral cortex in ApoE-/- mice. The number of the TNF-α-positive cells was markedly raised in the cerebral cortex after ApoE knockout, and the intensity of TNF-α positive substances in the hippocampus is higher in ApoE-/- mice than in wild-type mice. Conclusion The expressions of IL-1β and IL-8 in the brain increased after ApoE knockout in mice.
出处 《细胞与分子免疫学杂志》 CAS CSCD 北大核心 2015年第5期581-584,共4页 Chinese Journal of Cellular and Molecular Immunology
基金 国家自然科学基金(30570750 81401658) 安徽省教育厅自然科学基金(KJ2012A164)
关键词 载脂蛋白E基因敲除 炎症因子 apolipoprotein E knockout inflammatory factors brain
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参考文献22

  • 1van Es MA, van den Berg LH. Alzheimer's disease beyond APOE[J]. Nat genet, 2009,41 (10): 1047 -1048.
  • 2温蒲圆,罗浩,周丽,宋治,李闻文,周军.丹参酮ⅡA对阿尔茨海默病模型大鼠脑组织caspase-3、Akt与NF-κB表达的影响[J].细胞与分子免疫学杂志,2014,30(2):155-159. 被引量:15
  • 3Liu CC, Kanekiyo T, Xu H, et al. Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy[J]. Nat Rev Neurol, 2013, 9(2) : 106 -118.
  • 4Cramer PE, Cirrito m, Wesson DW, et al. ApoE-directed therapeutics rapidly clear f3-amyloid and reverse deficits in AD mouse models[J]. Science, 2012, 335(6075): 1503 -1506.
  • 5Jiang Q, Lee CY, Mandrekar S, et al. ApoE promotes the proteolytic degradation of Af3[J]. Neuron, 2008, 58(5): 681 -693.
  • 6张媛,孙源鸿,怀阳阳,张应玖.阿尔茨海默病治疗性单链抗体的研究进展[J].细胞与分子免疫学杂志,2014,30(12):1330-1334. 被引量:1
  • 7Palop 11, Mucke L. Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks[ll. Nat Neurosci, 2010, 13(7): 812 -818.
  • 8Sardi F, Fassina L, Venturini L, et al. Alzheimer's disease, autoimmmity and inllanmalion. The good, the bad and the ugly[J]. Autoimmun Rev, 2011, 11 (2) : 149 -153.
  • 9Takeda S, Sato N, Morishita R. Systemic inflammation, blood-brain barrier vulnerability and cognitive/non-cognitive symptoms in Alzheimer disease: relevance to pathogenesis and therapy[J/OL]. Front Aging Neurosci, 2014, 6: 171.
  • 10LynchJR, Morgan D, Mance 1. et al. Apolipoprotein E modulates glial activation and the endogenous central nervous system inflammatory response[J].J Neuroimmunol, 2001,114(112): 107 -113.

二级参考文献51

  • 1Taly A, Corringer PJ, Guedin D, et al. Nicotinic receptors: allosteric transitions and therapeurtic targets in the nervous system [J]. Nat Nev Drug Discov, 2009, 8(9) : 733 -750.
  • 2Beagley KW, Huston WM, Hansbro PM, et al. Chlamydial infection of immune eeUs: altered function and implications for disease[ J]. Crit Rev Immunol, 2009, 29(4) : 275 -305.
  • 3Hermindez F, de Barreda EG, Fuster-Matanzo A, et al. The role of GSK3 in Alzheimer Disease[J]. Brain Res Bull, 2009, 80(4/5) : 248 - 250.
  • 4Shang Q, Xu H, Huang L. Tanshinone II A: A promising natural cardioproteetive agent [ J/OA ]. Evid Based Complement Alternat Med, 2012, 2012: 716459.
  • 5Limpeanehob N, Jaipan S, Rattanakaruna S, et al. Neuroproteeive effect of Bacopa monnieri on beta-amyloid-induced cell death in primary cortical culture [ J ]. J Ethnopharmacol, 2008, 120 ( 1 ) : 112 -117.
  • 6Stephan A, Laroche S, Davis S. Generation of aggregated beta-a myloid in the rat hippocampus impairs synaptic transmission and plasticity and causes memory deficits[J]. J Neurosci, 2001, 21 (15) : 5703 -5714.
  • 7Zhang X, Wu M, Lu F, et al. Involvement of a7 nAChR signaling cascade in epigallocatechin gallate suppression of 13-amyloid-induced apoptotic cortical neuronal insults [ J]. Mol Neurobiol, 2013 Jun 27. [ Epnb ahead of print].
  • 8Hussain AR, Ahmed SO, Ahmed M, et al. Cross-talk between NF- ~B and the PI3-kinase/AKT pathway can be targeted in primary effusion lymphorna (PEL) cell lines for et~ciant apoptosis[ J/OA]. PLoS One, 2012, 7(6) : e39945.
  • 9Yu X, Pan Y, Ma H, et al. Simvastatin inhibits proliferation and induces apoptosis in human lung cancer cells[ J]. Oncol Res, 2013, 20(8) : 351 -357.
  • 10Tan L, Schedl P, Song HI, et al. The Toll-NFkappaB signaling pathway mediates the neuropathologieal effects of the human Alzheimer's Abeta42 polypeptide in Drosophila[ J/OA]. PLoS One, 2008, 3(12) : e3966.

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  • 1Krishnadas R,Nicol A,Sassarini J,et al. Circulating tumour necro- sis factor is highly correlated with brainstem serotonin transporter availability in humans [ J ]. Brain Behav Immun, 2015, pii ( 15 ) : 429 - 438.
  • 2Becker D, Deller T, Vlachos A. Tumor necrosis factor(TNF) -re- ceptor 1 and 2 mediate homeostatic synaptic plasticity of denervat- ed mouse dentate granule cells[ J]. Sci Rep,2015 ,5 :12726.
  • 3Miyatake S, Nonoguchi N, Furuse hi, et al. Pathophysiology, diag- nosis, and treatment of radiation necrosis in the brain [ J ]. Neurol Med Clair(Tokyo) ,2015,55( 1 ) :50 -59.
  • 4Opp MR, George A, Riuggold KM, et al. Sleep fragmentation and sepsis differentially impact blood-brain barrier integrity and trans- port of tumor necrosis factor-ct in aging[ J]. Brain Behav Irnmun, 2015, pii(15) :418 -423.
  • 5De Nuccio C, Bernardo A, Crueiani C ,et al. Peroxisome prolifera- tot activated rceeptor-'y agonists protect oligodendrocyte progeni- tors against tumor necrosis factor-alpha-induced damage: Effects on mitochondrial functions and differentiation [ J ]. Exp Neurol, 2015,271 (2) :506 -514.
  • 6Raivich G,Banati R. Brain microglia and blood-derived macropha- ges:molecular profiles and functional roles in multiple sclerosis and animal models of autoimmune demye!inating disease[ J ]. Brain Res Brain Res Rev,2004,46(3) :261 -281.
  • 7Thanasupawat T, Glogowska A, Burg M, et al. RXFP1 is targeted by complement Clq tumor necrosis factor-related factor 8 in brain cancer[ ] ]. Front Endocrinol ( Lausanne ) ,2015,6 ( 1 ) : 127 - 132.
  • 8Biesmans S, Bouwknecht JA, Ver Donck L, et al. Peripheral ad- ministration of tumor necrosis factor-alpha induces neuroinflam- mation and sickness but not depressive-jike behavior in mice [ J ]. Biomed Res Int,2015 ,2015 :716920.
  • 9Sonar S, Lal G. Role of tumor necrosis factor superfamily in neu- roinflammation and autoimmunity [ J ]. Front Immunol, 2015,6 (2) :364 -639.
  • 10Mishra P,Prasad KN ,Singh K,et al. Tumor necrosis factor-or and interleukin-1 f3 gene polymorphisms and risk of brain abscess in North Indian population [ J ]. Cytokine,2015,75 ( 1 ) : 159 - 1 64.

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