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羧基末端亚单位肽疫苗KLH-Aβ_(24-42)诱导正常BALB/c小鼠制备抗Aβ_(42)抗体

Inoculating subunit vaccine comprised of KLH and Aβ_(24-42) induced normal BALB/c mice to produce antibody against Aβ_(42)
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摘要 目的:探讨亚单位肽疫苗KLH-Aβ_(24-42)接种小鼠后特异性抗Aβ_(42)抗体的产生情况。方法:将Aβ_(24-42)羧基端与载体蛋白KLH结合制成亚单位肽疫苗免疫BALB/c小鼠。间接ELISA法检测其血清和脑匀浆上清液中的抗体滴度,HE染色对小鼠脑、肝、脾、心、肺和肾行形态学观察抗体毒性。结果:第2次接种后各实验组开始有血清抗体产生,抗体滴度随接种次数的增多而增高;但脑匀浆上清液中未检测到抗体;小鼠各主要脏器均未见病理性变化。结论:亚单位肽疫苗KLH-Aβ_(24-42)免疫BALB/c小鼠后能产生抗Aβ_(42)抗体,观察未见抗体对各重要脏器的毒性病理。 Objective: To study whether inoculating subunit vaccine comprised of carrier protein KLH and C terminal fragment Aβ24-42 could induce normal BALB/C mice to produce antibody against Aβ42 or not. Methods: The subunite vaccine comprised of KLH and Aβ24-42 was inoculated into BALB/c mice. Antibodies against Aβ42 of serum and superuatant of homogenated brain were assessed by indirect ELISA. The morphologies of brain, liver, spleen, heart, lung and kidney were observed in paraffin section by HE staining. Resuits: After the second inoculation,all experiment groups began to develop antibody against Aβ42, and the titer raised gradually with inoculating times. However, antibody against Aβ42 could not be detected in superuatant of homogenated brain. No morphological damages on the brain, liver, spleen, heart, lung and kidney were found out. Conclusion: BALB/c mice can be induced to develop antibody against Aβ42 after inoculating with subunite vaccine comprised of KLH and Aβ24-42, and there were rarely systematic toxicity in several important organs.
作者 李清 邬力祥
出处 《现代生物医学进展》 CAS 2008年第7期1236-1238,共3页 Progress in Modern Biomedicine
基金 湖南省重点学科建设项目资助(30770838)
关键词 亚单位肽疫苗 KLH—Aβ24-42 抗Aβ42抗体 peptide subunit vaccine KLH-Aβ24-42 antibody against Aβ42
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  • 1Schliebs R.Basal forebrain cholinergic dysfunction in Alzheimer's disease-interrelationship with beta-amyloid,inflam mation and neurotrophin signaling[J].Neurochem Res,2005,30(6-7):895-908
  • 2Eckert A,Marques CA,Keil U,Schossel K,Müller WE.Increased apoptotic cell death in sporadic and genetic Alzheimer's disease[J].Ann N Y Acad Sci,2003,1010:604-609
  • 3Dermaut B,Kumar-Singh S,Rademakers R,Theuns J,Cruts M,Van Broeckhoven C.Tau is central in the genetic Alzheimer-frontotemporal dementia spectrum[J].Trends Genet.2005 Dec,21(12):664-672
  • 4Shoghi-Jadid K,Small GW,Agdeppa ED,et al.Localization of neurofibrillary tangles and beta-amyloid plaques in the brains of living patients with Alzheimer disease[J].Am J Geriatr Psychiatry,2002,10(1):24-35
  • 5Hock C,Konietzko U,Streffer JR,et al.Antibodies against beta-amyloid slow cognitive decline in Alzheimer's disease[J].Neuron,200322,38(4):547-554
  • 6Mathis CA,Lopresti BJ,Klunk WE.Impact of amyloid imaging on drug development in Alzheimer's disease[J].Nucl Med Biol,2007,34(7):809-822
  • 7Schenk D.Amyloid-beta immunotherapy for Alzheimer's disease:the end of the beginning[J].Nat Rev Neurosci,2002,3(10):824-828
  • 8Horikoshi Y,Mori T,Maeda M,Kinoshita N,Sato K,Yamagnchi H.Abeta N-terminal-end specific antibody reduced beta-amyloid in Alzheimer-model mice[J].Biochem Biophys Res Commun,2004 10,325(2):384-387
  • 9Bard F,Barbour R,Cannon C,et al.Epitope and isotype specificities of antibodies to beta-amyloid peptide for protection against Alzheimer's disease-like neuropathology[J].Proc Natl Acad Sci USA,2003 18,100(4):2023-2028
  • 10Check E.Nerve inflammation halts trial for Alzheimer's drug[J].Nature,2002,415(6871):462

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