發(fā)布時(shí)間：2018-02-21 16:37

  本文關(guān)鍵詞： 硒 鋅 阿爾茨海默病 α、β、γ-分泌酶 Aβ- GSK-β Ph-tau 小鼠　出處：《營養(yǎng)學(xué)報(bào)》2017年02期 　論文類型：期刊論文

【摘要】：目的研究硒、鋅對老年性癡呆(Alzheimer’s,AD)模型小鼠酶解通路的保護(hù)作用及機(jī)制。方法選用健康雄性2月齡昆明種小鼠60只,隨機(jī)分為正常對照組(NC)、AD模型組、硒[Se,7.5μg/(kg bw)]+AD組、鋅[Zn,5 mg/(kg bw)]+AD組、硒[Se,7.5μg/(kg bw)]+鋅[Zn,5 mg/(kg bw)]+AD組、腦復(fù)康[Piracetam,230 mg/(kg bw)]+AD共6組,每組10只。連續(xù)60d腹腔注射D-半乳糖[150 mg/(kg bw)],建立老年性癡呆模型,采用酶聯(lián)免疫吸附測定法(enzyme linked immunosorbent assay,ELISA)檢測血清中α、β、γ-分泌酶含量以及腦組織中Aβ1-40含量;Western-blot法檢測腦組織中糖原合成酶激酶-3β(GSK-3β)和磷酸化Tau(Ph-tau)蛋白水平。結(jié)果 ELISA法顯示,與AD組比較,硒、鋅可以增強(qiáng)α-分泌酶活性,抑制β、γ-分泌酶的活性,且硒鋅聯(lián)合作用增強(qiáng),腦組織中Aβ_(1-40)含量明顯降低。Western-blot法檢測顯示,與NC組比較,AD模型組GSK-3β、Ph-tau蛋白表達(dá)水平升高,而硒、鋅處理組和硒鋅聯(lián)合作用組,GSK-3β、Ph-tau蛋白表達(dá)水平明顯降低。結(jié)論硒、鋅通過增加內(nèi)源性α-分泌酶的活性,抑制β、γ-分泌酶的活性,減少Aβ_(1-40)的生成,降低GSK-3β、Ph-tau蛋白表達(dá)水平,可能對AD的發(fā)病及進(jìn)展有一定預(yù)防保護(hù)作用。
[Abstract]:Objective to study the protective effect and mechanism of selenium and zinc on enzymatic pathway in mice with Alzheimer's disease (AD). Methods 60 healthy male 2 month old Kunming mice were randomly divided into three groups: normal control group, AD group, AD group and Zn [Zn5 mg/(kg bww] AD group. The Alzheimer's disease model was established by intraperitoneal injection of D-galactose (150 mg/(kg BW) for 60 days in 6 AD groups, 10 rats in each group, and 10 rats in each group in the AD group [Zn5 mg/(kg BW] and Piracetamol 230 mg/(kg bww, respectively, for 60 consecutive days, in order to establish the Alzheimer's disease model, and to establish the model of Alzheimer's disease by intraperitoneal injection of D-galactose (150 mg/(kg BWW) for 60 days. The levels of 偽, 尾, 緯 -secretory enzymes in serum and A 尾 _ 1-40 in brain tissue were detected by enzyme linked immunosorbent assayayesis-ELISA-Western-blot method was used to detect the protein levels of glycogen synthase kinase -3 尾 -PhosphorylTau-Ph-tau.Results compared with AD group, the levels of se, se, Tau-tau-tauprotein were detected by ELISA. Zinc could increase the activity of 偽 -secretase, inhibit the activity of 尾, 緯 -secretase, and increase the combined effect of selenium and zinc. The content of A 尾 -tir 1-40) in brain tissue was significantly decreased. Western-blot assay showed that the expression of GSK-3 尾 -Ph-tau protein in AD model group was higher than that in NC group. Conclusion the level of GSK-3 尾 -Ph-tau protein in zinc treated group and Se-Zn combined treatment group was significantly decreased. Conclusion selenium and zinc can inhibit the activity of 尾, 緯 -secretase, reduce the production of A 尾 -1-40) and decrease the expression level of GSK-3 尾 -Ph-tau protein by increasing the activity of endogenous 偽 -secretase, reducing the activity of 尾, 緯 -secretase, and decreasing the expression level of GSK-3 尾 -Ph-tau protein. It may have a preventive and protective effect on the pathogenesis and progression of AD.
【作者單位】： 延邊大學(xué)醫(yī)學(xué)院預(yù)防醫(yī)學(xué)教研室;
【基金】：吉林省教育廳科學(xué)技術(shù)研究項(xiàng)目(吉教科合字2016-279號(hào))
【分類號(hào)】：R-332;R749.16

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1 趙保勝;劉勇;艾路;;老年性癡呆模型的建立方法[A];2009年全國中藥學(xué)術(shù)研討會(huì)論文集[C];2009年

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