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尼古丁暴露对成年昆明小鼠大脑内Presenilin 1表达的影响

The effect of nicotine exposure to the expression of presenilin 1 in the cerebrum of adult kunming mice
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摘要 目的探讨尼古丁暴露对成年昆明小鼠大脑内Presenilin 1(PS1)表达的影响。方法 SPF级雄性成年昆明种小鼠50只,随机分为对照组,生理盐水组、尼古丁组,尼古丁组依据注射尼古丁溶液时间再细分为Tes1(10d)、Tes2(20d)、Tes3(40d),应用RT-PCR和Western blot方法分别检测小鼠大脑内PS1 mRNA和PS1蛋白表达情况,免疫组织化学染色方法检测PS1在小鼠大脑内表达的部位。结果免疫组织化学检测发现,对照组中的大脑皮层、海马细胞层和第三脑室周围有大量PS1阳性细胞分布,在海马细胞层之间的纤维区域有PS1阳性反应物集聚。尼古丁组仅见第三脑室周围有较多PS1阳性细胞分布,RT-PCR和Western blot方法检测发现,尼古丁组中PS1 mRNA和PS1蛋白表达水平都明显低于对照组和生理盐水组(P<0.05)。结论尼古丁暴露可以抑制成年昆明小鼠大脑皮层、海马细胞层、海马细胞层之间纤维区域中PS1的表达。 Objective To study the effect of nicotine exposure to the expression of presenilin 1(PS1) in the cerebrum of adult kunming mice. Methods 50 SPF level male adult Kunming mice were randomly divided into Control, Saline, nicotine groups(injected with nicotine solution 0.1ml, 3mg/kg for 10 days, for 20 days and for 40 days respectively)to establish models of nicotine exposure. The expression of PS1 was observed by immunohistochemical staining and Western blot and RT-PCR. Results A lot of PS1 positive cells and nerve fibers distributing in the cortex, hippocampus and the area around the third ventricle in control and saline groups, whereas PS1 positive cells were only found in the domain of the periphery of the third ventricle in nicotine group. The expression levels of PS1 protine and mRNA decreased significantly in nicotine groups than in control and saline groups by western blot and RT-PCR respectively. Conclusion The exposure of nicotine inhibits the expression of PS1 in the cortex and hippocampus selectively in Kunmin mice.
出处 《解剖科学进展》 CAS 2012年第6期537-540,共4页 Progress of Anatomical Sciences
基金 国家自然科学基金资助项目(No.31040038)
关键词 尼古丁 PRESENILIN 1 大脑 昆明小鼠 Nicotine Presenilin 1 cerebrum Kunmin mice
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参考文献13

  • 1Selkce DJ. Al:eimer' s disease: genes, pmteirrs, and therapy[J]. Physiological Rev, 2001, 81 (2): 741-760.
  • 2De Strooper B. Aph-1, Pen-2, and Nicastrin with Presenilin generate an active gamma-Secretase complex[J]. Neuron, 2003, 38: 9-12.
  • 3Jiang S, Zhan4g M, Ren D, et al. Enhanced production of amyloid preeursor protein mRNA by peripheral mononuclear blood cell in Alzheimer's di:ase[J]. Am J Med Genet B Neuropsychtr Genet, 2003, 118( 1): 99-102.
  • 4Hen'eman A, Serneels L, Annaert W, et al. Total inactivation of β- secretase activity in presenilin-deficient embryonic stem cells[J]. Nat Cell Biol, 2002, 2: 461-462.
  • 5Wenk GL, Quack G, Moehius H J, et al. No interaction of memantine with acetylcholinescerase inhibitors approved for clinical use[J]. Life Sci, 2000, 66(12): 1079-1083.
  • 6Brenner DE, Kukull WA, van Belle G, et al. Relationship between cigaretle smoking and Alzheimer' s disease in a pepulationbased case-control study[J]. Neurology, 1993, 43: 293-300.
  • 7Zhao Y, Liu W, Guo C. Establishment of rat models with ALzheimer's disease induced by β -Amyloid proteinand effects of Nicotine on the animal models[J]. J Shanghai Jiaotong University (Medical Science), 2006, 26(7): 719-724.
  • 8Ewa HL, Jennifer C, Jessica K, et al. Nicotine reduce A β in the brain and cerebral vessels of APPsw mice[J]. Eur J Neurosci, 2004, 19: 2703-2710.
  • 9Takasugi N, Tomita T, Hayashi I, et al. The role of presenilin cofactors in the gamma-secretase complex[J]. Nature, 2003, 27, 422(6930): 438- 441.
  • 10Wisniewlki T. S182 protein in Alzheimer' s neurite plaques[J]. Lancet, 1995, 346: 1366.

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