期刊文献+

丹参酮ⅡA对Aβ_(1-42)处理的体外培养海马脑片组织神经元与胶质细胞的影响 被引量:5

Effect of tanshinone Ⅱ A on the expressions of NeuN,GFAP and CD11b in Aβ_(1-42) induced newborn rat hippocampal slices in vitro
下载PDF
导出
摘要 目的观察丹参酮ⅡA(TanⅡA)干预Aβ1-42处理体外培养的新生大鼠海马脑片组织中神经元特异核蛋白(NeuN)、胶质纤维酸性蛋白(GFAP)和CD11b表达的影响。方法将大鼠海马脑片随机分为正常对照组、Aβ高、低剂量模型组和Aβ模型组联合TanⅡA高、低剂量组,共7组。其中正常组仍用完全培养液培养,Aβ高剂量模型组为完全培养基加5μg Aβ1-42,Aβ低剂量模型组为完全培养基加0.5μg的Aβ1-42,TanⅡA药物处理组分别为Aβ模型组加8μg或16μg TanⅡA。免疫组织化学染色法检测TanⅡA处理后各组NeuN、GFAP和CD11b表达水平的改变。结果与正常对照组比较,不同剂量Aβ处理组NeuN表达均减少,其中高剂量组下降明显(P<0.05),用高剂量TanⅡA干预后NeuN表达量均显著上升(P<0.05);对比正常对照组,Aβ处理组中GFAP和CD11b表达量均上升,其中高剂量Aβ处理组中两种蛋白表达量显著增高(P<0.05),TanⅡA处理组2种蛋白表达均下降,高剂量组下降明显(P<0.05)。结论 TanⅡA干预Aβ诱导的AD海马脑片模型,可有效的减少组织中GFAP和CD11b的表达水平,抑制胶质细胞的活化。 [ Abstract] Objective To detect the expressions of neuron-specific nuclear protein (NeuN), glial fibrillary acidic protein (GFAP) and CDIIb in the Aβ1- 42 induced newborn rat hippocampal slices in vitro and investigate the neuroprotective effect of tanshinone ]] A. Methods Hippocampal slices were randomly divided into ? groups: normal control group; Aβ1- 42 (5.0, 0. ,5 iJg/mL) groups; Aβ(5.0 iJg/mL) + low or high (8.0 mg or 16 mg) doses of Tan HA groups,Aβ (0.5 pg/mL) + low or high (8.0 mg or 16 mg) doses of Tan Ⅱ A groups. The expression levels of GFAP, NeuN and CDllb were detected by immunohistochemistry. Results Compared with the control group, the expression of NeuN decreased in the two different doses of Aβ1- 42 groups, especially in the high-dose group (P 〈 0.05 ) ; while the level significantly increased after high-dose Tan H A treatment (P〈O. 05). Compared with the control group, the expression levels of GFAP and CDllb increased in the two different doses of Aβ1- 42 groups, and the levels in the high-dose group were the highest ( P 〈 0. 05 ) ; while the levels were reduced significantly by Tan HA treatment, the more by the high-dose TanⅡA ( P 〈0. 05). Conclusion Tan HA can down- regulate the levels of GFAP and CDIlb and inhibit the activity of glial cells in rat hippocampal slices induced by Aβ1- 42 in vitro.
出处 《细胞与分子免疫学杂志》 CAS CSCD 北大核心 2013年第11期1150-1154,共5页 Chinese Journal of Cellular and Molecular Immunology
基金 湖南省自然科学基金(07JJ5042) 湖南省科技厅计划项目(2011WK3047) 中南大学贵重仪器设备开放共享基金(csuzu2013041)
关键词 丹参酮ⅡA 阿尔茨海默病 神经元特异核蛋白 胶质纤维酸性蛋白 CD11B tanshinone Ⅱ A Alzheimer's disease NeuN GFAP CDllb
  • 相关文献

参考文献16

  • 1Kreutz F, Frozza RL, Brcier AC, et al. Amyloid-13 induced toxicity involves ganglioside expression and is sensitive to GM1 neuroprotective action[J]. Neurochem Int, 2011, 59(5) : 648 -655.
  • 2Nelson PT, Braak H, Markesbery WR. Neuropathology and cognitive impairment in Alzheimer disease: a complex but coherent relationship [J]. J Neuropathol Exp Neurol, 2009, 68(1) : 1 -14.
  • 3Zhou J, Fonseca MI, Kayed R, et al. Novel AI3 peptide immunogens modulate plaque pathology and inflammation in a murine model of Alzheimer~ disease[ J/OA]. J Neureinflammatian, 2005, 2: 28.
  • 4Nassif M, Hoppe J, Santin K, et al. Beta-amyloid peptide toxicity in organotypic hippocampal slice culture involves Akt/PKB, GSK-3beta, and PTEN[J]. Neurochem lnt, 2007, 50(1) : 229 -235.
  • 5Bergamasehini L, Canziani S, Bottasso B, et al. Alzheimer's beta- amyloid pepfides can activate the early components of complement classical pathway in a Clq-independent manner[ J ]. Clin Exp lmmunol, 1999, 115(3) : 526 -533.
  • 6Zhu B, Zhai Q, Yu B. Tanshinone HA protects rat primary hepatoeytes against carbon tetrachloride toxicity via inhibiting mitochondriapermeability transition [ J ]. Pharm Biol, 2010, 48 ( 5 ) : 484 - 487.
  • 7Nam JH, Park KW, Park ES, et al. Interleukin-13/-4-induced oxidative stress contributes to death of hippocampal neurons in al31 _4z-treated hippocampus in v/vo[J]. Antioxid Redox Signal, 2012, 16(12) : 1369 - 1383.
  • 8周军,周丽,曾庆仁,侯德仁,陈坤,田怡,万顺.丹皮酚对AD模型鼠脑组织神经细胞与胶质细胞活性的影响[J].中成药,2010,32(9):1594-1597. 被引量:4
  • 9Stoppini L, Buchs PA, Mu|ler D. A simple method for organotypic cultures of nervous tissue [ J ]. J Neurosci Methods, 1991, 37 ( 2 ) : 17'~ - lg2.
  • 10Kim H, Kim E, Park M, et al. Organotypic hippocampal slice culture from the adult mouse brain: a versatile tool for translational neuropsychopharmacology [ J ]. Prog Neuropsychopharmacol Biol Psychiatry, 2013,41 : 36 -43.

二级参考文献12

  • 1张洁,曾晓荣,杨艳,刘智飞.丹参酮ⅡA磺酸钠和丹参素对猪冠状动脉平滑肌细胞钙激活钾通道的激活机制[J].中国药理学与毒理学杂志,2005,19(4):270-273. 被引量:39
  • 2Yuan J, Yankner BA, Apoptosis in the neverous system [ J]. Nature, 2000, 407 (6805) : 802-809.
  • 3Ye L, Qiao J T, Suppressive action produced by beta-amyloid peptide Fragment 31-35 on long-term potentiation in rat hippo- campus is N-methyl-D-aspartate receptor-independent: it's offset by huperzine A [J]. Neurosci Lett, 1999,275 (3) : 187-190.
  • 4Fiala M, Zhang L, Gan X, et al. Amyloid beta induces chemokine secretion and monocyte migration across a human blood brain barriermodel[J]. J Mol Med, 1998,4(7) :4802489.
  • 5Huang X D, A twood C S, Hurtshorn M A, et al. The Aβ peptide of Alzheimer' s disease directly produces hydrogen peroxide through metal ion reduction [ J ]. Biochemistry, 1999,38 : 7609- 7616.
  • 6Zhang J M, Wu M N, Qi J S, et al. Amyloid beta protein fragment 31-35 suppresses long term potentiation in hippocampal CA1 region of rats in vivo[J]. Synapse, 2006,60(4) :307-313.
  • 7Freir D B, Holscher C, Herron C E. Blockade of long-term potentiation by beta amyloid peptides in the CAI region of the rat hippocampus in vivo [ J]. J Neurophysiol, 2001,85 ( 3 ) : 708- 713.
  • 8Goodison K L, Parhad M, White C L, et al. Neuronal and glial gene expression in neoeortex of Down ' s syndrome and Alzheimer' s disease [ J]. J Neuropathol Exp Neurol, 1993,52 : 192- 198.
  • 9Li Y, Wang J, Sheng J G, et al. S beta increase levels of beta amyloid precursor protein and its encoding mRNA in rat neuronal cultures[ J ]. J Neurochem, 1998,71 : 1421-1428.
  • 10Mrak R E, Sheng J G,Griffin W S. Grial cytokines in Alzheimer's disease Review and pathogenic implication [J]. Hum Pathol, 1995,26:816-823.

共引文献3

同被引文献38

引证文献5

二级引证文献22

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部