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作 者:黎荣[1] 魏斌[2] 徐灵源[3] 李勇文[1] 段小群[1]
机构地区:[1]桂林医学院,广西桂林541004 [2]广西壮族自治区妇幼保健院,南宁530021 [3]右江民族医学院附属医院,广西百色533000
出 处:《中国实验方剂学杂志》2013年第4期259-262,共4页Chinese Journal of Experimental Traditional Medical Formulae
摘 要:目的:研究葛根素对6-羟多巴胺(6-OHDA)致帕金森病大鼠黑质神经生长因子(NGF),即刻早期基因(c-fos,c-jun)mRNA表达的影响。方法:建立帕金森病大鼠模型,随机分成6组:正常组、模型组、左旋多巴阳性组及葛根素低、中、高剂量组,并设立正常组。ig给予葛根素20,40,80 mg.kg-1,阳性组给予左旋多巴40 mg.kg-1,连续灌胃30 d。Nissl染色观察黑质神经细胞尼氏小体的变化,免疫组织化学法检测黑质组织神经生长因子(NGF)表达。原位杂交法检测c-fos,c-jun mRNA表达。结果:与正常组比较,模型组帕金森病大鼠黑质神经细胞严重损伤以及NGF,c-fos,c-jun表达明显减少(P<0.01)。与模型组比较,葛根素有效地增加黑质组织神经细胞尼氏小体数量。增加黑质组织中NGF阳性细胞数量(139.1±26.5),(206.1±33.8),(294.6±40.7)cell.mm-2(P<0.01)。同时明显上调c-fos,c-jun mRNA表达(98.5±16.4),(137.6±19.5),(205.4±28.9);(90.6±15.3),(125.9±18.6),(191.7±27.5)cell.mm-2(P<0.01)。结论:葛根素对6-OHDA所致PD大鼠黑质具有神经保护作用,机制可能与其调节c-fos/c-jun表达而介导神经修复和增强信号传导有关。Objective: To investigate the effect of puerarin on the expressions of nerve growth factor (NGF) , c-fos, c-jun in substantia nigra of Parkinson's rats induced by 6-hydroxydopamine (6-OHDA). Method: Parkinson's rat model was established, model rats were randomly divided into 5 groups: model group, L-dopa group (40 mg .kg-1 ) , low-, medium-and high-dosage groups of puerarin (20, 40, 80 mg kg-1 ). The drugs were intragastrically perfused to rats daily for 30 days. The changes of nissl bodies in nerve cells of substantia nigra were observed by Nissl staining. The expression of NGF was tested by immunohistochemistry assay. And the c-fos, c-jun mRNA levels were tested by in situ hybridization analysis. Result: Compared to model group, the neuronal cells were badly injured and expression of NGF, c-fos, c-jun mRNA was obviously reduced in substantia nigra of PD rats in model group. Compared to model group, puerarin effectively increased nissl bodies in neuronal cells of substantia nigra of PD rats, and elevated the number of NGF-immunoreactive cells in substantia nigra (P 〈 0.01 ). The expressions of c-fos, c-jun mRNA were significantly up-regulated. Conclusion: The results demonstrate that puerarin has a neuroprotection on the neuronal cells in substantia nigra of PD rats induced by 6-OHDA, though the underlying mechanisms that may be associated with regulation of c-fos/c-jun expressions to mediate neuronic repairment and enhance the signaling transduction.
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