开心散对快速老化痴呆小鼠SAMP8炎症因子及β-APP影响随机平行对照研究
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摘要
[目的]观察开心散对快速老化痴呆小鼠SAMP8炎症因子及β-APP影响。[方法]使用随机平行对照方法,将40只SAMP8小鼠按随机数字标法分为4组,10只/组,模型对照组、开心散组(高、低剂量组)、艾地苯醌组。正常对照组10只SAMR1小鼠。采用ELISA双抗体夹心法测定干预后脑组织及血清TNF-α、IL-8和β-APP含量。[结果]与正常对照组比较,模型组小鼠脑组织TNF-α、IL-8和β-APP含量明显升高(P<0.01),血清TNF-α、IL-8和β-APP浓度明显降低(P<0.01);与模型组比较,开心散低剂量组、开心散高剂量组小鼠脑组织TNF-α、IL-8和β-APP含量明显降低(P<0.01),血清TNF-α、IL-8和β-APP浓度明显升高(P<0.01)。[结论]开心散可减少脑组织的β-APP含量,降低炎症因子TNF-α、IL-8水平。
[Objective]Effect of kaxin-san on inflammatory factor andβ-APP of senescence accelerated mouse/prone 8(SAMP8). Methods:By random parallel control method,40 SAMP8s were randomly divided into the model group,high-does kaxin-san group,low-does kaxin-san group and idebenone group,10 rats in each group. 10 SAMR1s were adopted as normal control group. The levels of TNF-α,IL-8and β-APP in brain tissue and serum of SAMP8 by double antibody enzyme linked immunosorbent assay(ELISA).Results:Compared with control group,the contents of TNF-α,IL-8 and β-APP in brain tissue of model group was increased(P<0.01),the concentration of TNF-α,IL-8 and β-APP in serum of model group was decreased(P<0.01);Compared with model group,the contents of TNF-α,IL-8 and β-APP in brain tissue of high-does kaxin-san group,low-does kaxin-san group was decreased(P<0.01),the concentration of TNF-α,IL-8 andβ-APP in serum of high-does kaxin-san group,low-does kaxin-san group was increased(P<0.01). Conclusion:kaxin-san can exert neuroprotective effects by decrease the contents of TNF-α,IL-8 and β-APP in brain tissue.This may be important mechanisms of kaxin-san in improving the abilities of learning and memory.
[Objective]Effect of kaxin-san on inflammatory factor andβ-APP of senescence accelerated mouse/prone 8(SAMP8). Methods:By random parallel control method,40 SAMP8s were randomly divided into the model group,high-does kaxin-san group,low-does kaxin-san group and idebenone group,10 rats in each group. 10 SAMR1s were adopted as normal control group. The levels of TNF-α,IL-8and β-APP in brain tissue and serum of SAMP8 by double antibody enzyme linked immunosorbent assay(ELISA).Results:Compared with control group,the contents of TNF-α,IL-8 and β-APP in brain tissue of model group was increased(P<0.01),the concentration of TNF-α,IL-8 and β-APP in serum of model group was decreased(P<0.01);Compared with model group,the contents of TNF-α,IL-8 and β-APP in brain tissue of high-does kaxin-san group,low-does kaxin-san group was decreased(P<0.01),the concentration of TNF-α,IL-8 andβ-APP in serum of high-does kaxin-san group,low-does kaxin-san group was increased(P<0.01). Conclusion:kaxin-san can exert neuroprotective effects by decrease the contents of TNF-α,IL-8 and β-APP in brain tissue.This may be important mechanisms of kaxin-san in improving the abilities of learning and memory.
引文
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[3]Mc Donald JM,Savva GM,Brayne C,et al.The presence of sodium dodecyl sulphate-stable Abeta dimers is strongly associated with Alzheimer-type demen-tia[J].Brain,2010,133(Pt 5):1328-1341.
[4]曾凡,张吉强,王延江.等.体液生物标记物在阿尔茨海默病早诊断中的作用与评价[J].中国神经精神疾病杂志,2011,37(4):244-246.
[5]Small SA,Gandy S.Sorting through the cell biology of Alzheimer′s disease:intracellular pathways to pathogenesis[J].Neuron,2006,52(1):15-31.
[6]Stein TD,Anders NJ,DeCarli C,et al.Neutralization of transthyretin reverses the neuroprotectiveefects of secreted amyloid precursor protein(APP)in APPsw mice resulting in tau phosphorylation and loss of hippocampal neurons:support for the amyloid hypothesis[J].J Neurosci,2004,24(35):7707-7717.
[7]Tebbenkamp AT.Borchelt DR.Protein aggregate characterization in models of neurodegenerative disease[J].Methods Mol Biol,2009,(566):85-91.
[8]Takaheshi M,Dore S,Ferris CD,et al.Amyloid precursor proteins inhibit heme oxygenase activity and angment neurotoxicity in Alzheimer’s disease[J].Neuron,2000,(28):461-473.
[9]Selkoe DJ.Alzheimer’s disease:genes,proteins,and therapy[J].Physiol Rev,2001,(81):741-766.
[10]Neary JT,Kang Y.Signaling from P2 Nucleotide recep tors to protein kinase cascades indued by CNS jnjury implications for reactive gliosis and Neurodegen-eration[J].Mol Neurobiol,2005,(1-3):95-103.
[11]Markiewicz I,Lukomska B,The role of astrocytes in the physiology and pathology of the central nervous system[J].Acta Neurobio Exp,2006(,4):343-358.
[12]Aisen PS.The inflammatory hypothesis of Alzheiner disease:dead or alive[J].Alzheimer Dis Assoc Discord,2008,(22):4-5.
[13]于恺,张强,韩杰.阿尔茨海默病患者血清和脑脊液中肿瘤坏死因子α及白细胞介素8的水平[J].中国临床康复,2005,9(45):21-23.
[14]韩杰,李明,郑莉莎.阿尔茨海默病患者血清与脑脊液中多种细胞因子的研究[J].中华老年心脑血管病杂志,2005,7(2):112-114.
[15]曾毅丹,黄芳,汪家梨.开心散现代药理作用的研究[J].海峡药学,2006,18(5):12-14.
[16]温薇,张超,刘明.等.开心散含药血清对Aβ诱发的PC12细胞损伤的改善作用[J].中医药信息,2012,29(4):80-81.
[17]张冲,程锦雁,陈清轩.动物模型SAM小鼠及其在老年医学研究中的应用[J].实验动物科学与管理,2002,19(4):26-32.