本文選題：缺鋅　切入點(diǎn)：海馬神經(jīng)細(xì)胞　出處：《營養(yǎng)學(xué)報》2017年04期 　論文類型：期刊論文

【摘要】：目的觀察鋅缺乏致原代培養(yǎng)的大鼠海馬神經(jīng)細(xì)胞損傷中DNA甲基化及組蛋白去乙�；嚓P(guān)酶的變化,對缺鋅致海馬神經(jīng)細(xì)胞損傷的表觀遺傳機(jī)制進(jìn)行初探。方法將原代培養(yǎng)的大鼠海馬神經(jīng)細(xì)胞隨機(jī)分為對照(control);缺鋅[四吡啶甲基乙二胺,N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine,TPEN];補(bǔ)鋅5和50μmol/L(TPEN+5μmol/L Zn SO_4,TPEN+50μmol/L Zn SO_4)4組,除對照組不加任何處理外,其余3組分別在培養(yǎng)液中加入2μmol/L TPEN,補(bǔ)鋅組則對應(yīng)加入5和50μmol/L Zn SO_4,作用24h。MTT法檢測細(xì)胞存活率;免疫酶學(xué)法檢測HDAC活性;RT-PCR法檢測DNA甲基轉(zhuǎn)移酶(DNMT3a、DNMT3b)及組蛋白去乙�；窰DACs(HDAC1、HDAC2、HDAC3)的m RNA表達(dá)水平。結(jié)果與對照組比較,(1)缺鋅組海馬神經(jīng)存活率明顯降低(P0.05);5μmol/L補(bǔ)鋅和50μmol/L補(bǔ)鋅均可顯著抑制TPEN誘導(dǎo)的細(xì)胞存活率降低(P0.05)。(2)缺鋅組海馬神經(jīng)細(xì)胞內(nèi)DNMT1 m RNA的表達(dá)明顯上調(diào),DNMT3a m RNA的表達(dá)明顯下調(diào)(P0.05),而5μmol/L補(bǔ)鋅組或50μmol/L補(bǔ)鋅組均能夠顯著抑制TPEN誘導(dǎo)的DNMT1 m RNA和DNMT3a m RNA表達(dá)異常(P0.05)。與對照組比較,缺鋅組海馬神經(jīng)細(xì)胞內(nèi)DNMT3b m RNA的表達(dá)無明顯變化(P0.05),與對照組比較,50μmol/L補(bǔ)鋅后,DNMT3b m RNA表達(dá)明顯上調(diào)(P0.05)。(3)缺鋅組海馬神經(jīng)細(xì)胞內(nèi)HDAC活性及HDAC2的m RNA表達(dá)明顯升高(P0.05),HDAC1及HDAC3 m RNA的表達(dá)無明顯變化(P0.05);補(bǔ)鋅能顯著抑制TPEN誘導(dǎo)的HDAC活性及HDAC2 m RNA表達(dá)異常(P0.05)。結(jié)論細(xì)胞內(nèi)缺鋅誘導(dǎo)海馬神經(jīng)細(xì)胞損傷,造成DNA甲基化和組蛋白去乙�；揎椀母淖儭�
[Abstract]:Objective to observe the changes of DNA methylation and histone deacetylation related enzymes in primary cultured rat hippocampal neurons injured by zinc deficiency. Methods the primary cultured rat hippocampal neurons were randomly divided into three groups: control control group; zinc deficiency group [tetramethylenediamineurium pyridylmethyldiethylenediamine]; zinc supplementation (5 渭 mol/L(TPEN) and 50 渭 mol/L(TPEN 5 渭 mol/L ZnSO4 / TPEN 50 渭 mol/L Zn SO_4)4 group. In addition to the control group without any treatment, 2 渭 mol/L TPEN was added into the culture medium in the other three groups, and the zinc supplementation group was supplemented with 5 and 50 渭 mol/L ZnSSO4 respectively. The survival rate of the cells was measured by 24 h. The expression of m RNA in DNA methyltransferase (DNA) and histone deacetylase (HDAC1HDAC2HDAC3) was detected by RT-PCR and immunoenzymatic assay. Results compared with the control group, the survival rate of hippocampal nerve in the zinc-deficient group was significantly lower than that in the control group. The survival rate of hippocampal nerve in the zinc-deficient group was significantly lower than that in the zinc-deficient group. The expression of DNMT1 m RNA in hippocampal neurons of zinc-deficient group was significantly up-regulated and down-regulated P0.05 RNA expression, while 5 渭 mol/L zinc supplementation group or 50 渭 mol/L zinc supplementation group could significantly inhibit TPEN induced DNMT1. The expression of m RNA and DNMT3a m RNA was abnormal (P 0.05). There was no significant change in the expression of DNMT3b m RNA in hippocampal neurons in zinc-deficient group. Compared with the control group, the expression of DNMT3b m RNA increased significantly after zinc supplementation with 50 渭 mol/L. The activity of HDAC and the expression of m RNA of HDAC2 in hippocampal neurons of zinc-deficient group significantly increased HDAC1 and HDAC3 m. Zinc supplementation can significantly inhibit the HDAC activity induced by TPEN and the abnormal expression of HDAC2 m RNA. Conclusion Zinc deficiency can induce hippocampal nerve cell injury. Changes in DNA methylation and histone deacetylation were caused.
【作者單位】： 軍事醫(yī)學(xué)科學(xué)院衛(wèi)生學(xué)環(huán)境醫(yī)學(xué)研究所;成都軍區(qū)疾病預(yù)防控制中心;
【基金】：天津市應(yīng)用基礎(chǔ)與前沿技術(shù)研究計劃(No.15JCYBJC27100) 國家自然科學(xué)基金(No.30901185)
【分類號】：R151

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