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作 者:黎荣[1] 徐灵源[2] 梁韬[3] 张士军[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]右江民族医学院附属医院药剂科,广西百色533000 [3]广西医科大学,南宁530021
出 处:《中国实验方剂学杂志》2013年第2期247-250,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(PD)模型大鼠黑质组织神经细胞的保护作用。方法:建立帕金森病大鼠模型,随机分成5组:模型组、左旋多巴阳性组及葛根素低、中、高剂量组。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。检测黑质组织中谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性以及丙二醛(MDA)含量,进行黑质神经细胞常规染色观察,Western blot法检测黑质组织内诱导型一氧化氮合酶(iNOS)、环-磷酸腺苷(cAMP)反应元件结合蛋白(CREB)蛋白表达。结果:葛根素能缓解帕金森模型大鼠病情。与模型组比较,葛根素有效增加帕金森病大鼠黑质组织中GSH-Px,SOD活性,同时降低MDA含量(P<0.01)。下调黑质组织中iNOS蛋白水平,并上调CREB蛋白表达(P<0.01)。结论:葛根素对6-羟基多巴胺所致PD大鼠黑质组织神经细胞具有保护作用,机制可能与其抑制过氧化应激作用以及调节内源性iNOS、CREB蛋白的表达有关。Objective: To investigate the effect of puerarin on parkinson'as rats model induced by 6- hydroxydopamine (6-OHDA). Method: Parkinson's rats model was established, the 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 consecutive days. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) as well as the contents of MDA in substantia nigra tissue were tested by biochemical method ; the pathological change of nerve cells in substantia nigra was observed by HE staining; then the expressions of induced nitric oxide synthase ( iNOS), cyclic adenosine monophosphate (cAMP) -response-element-binding-protein (CREB) in substantia nigra were using Western blot analysis. Result: The condition of Parkinson's rats model was alleviated via puerarin treatment. Compared to model control group, puerarin significantly elevated the activities of GSH-Px and SOD in substantia nigra tissue of parkinson'as rats, while the MDA contents was reduced (P 〈 0.01 ) ; and down-regulated the iNOS protein level in substantia nigra tissue, while the expression of CREB was increased (P 〈 0.01 ). Conclusion: The findings indicate that puerarin has protective effect on the 6-OHDA-induced PD rats the mechanism may be associated with restraining the oxidative stress and regulations of endogenous iNOS, CREB expressions.
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