吕小生;陈旭义;汤锋武;张赛;蒋显锋;
LV Xiaoshen1,CHEN Xuyi2,TANG Fengwu2,ZHANG Shai2,JIANG Xianfeng2(1.Department of Cerebral Surgery,Leting County Hospital,Tangshan 063000,Hebei,China;2.Department of Cerebral Surgery,the Affiliated Hospital of Logistics Academy of the Armed Police Force,Dongli area 300162,Tianjin,China)

• 1:唐山市乐亭县医院外四科
• 2:武警后勤学院附属医院脑系科

摘要(Abstract)：

目的:研究腺嘌呤核苷酸转位酶1(ANT1)在亚硒酸钠抑制脑胶质瘤生长中的作用机制。方法:将不同浓度的亚硒酸钠(0.5、1.0、2.0、4.0μmol/L)侵染人脑胶质瘤细胞SHG44,MTT比色法检测亚硒酸钠对SHG44的增殖的影响;PCR法检测ANT1的表达;提取细胞线粒体后通过观察线粒体的荧光强度,检测SHG44的线粒体膜电位和膜通道开放程度。结果:亚硒酸钠对人脑胶质瘤细胞具有明显的抑制作用,2.0及4.0μmol/L染硒组差异均有统计学意义(P<0.05),ANT1的表达在各染硒组均出现显著性增加(P<0.05);线粒体膜电位在2.0及4.0μmol/L染硒组显著降低(P<0.05),线粒体膜通道转运孔开放程度在1.0、2.0及4.0μmol/L组显著增高(P<0.05)。结论:亚硒酸钠能抑制人脑胶质瘤细胞SHG44地生长,并伴随线粒体膜电位降低和线粒体膜通道转运孔开放程度增加,ANT1可能参与了其作用机制。
Objective: To study the mechanism of adenine nucleotide translocator 1 in the inhibition of sodium selenite to human glioma SHG44 cell.Methods: SHG44 cells were treated with different concentrations of sodium selenite(0.5,1.0,2.0 and 4.0 μmol/L).Growth inhibition of SHG44 cells was detected by MTT assay.Expression of ANT1 was detected by PCR method.Mitochondrial permeability transition and mitochondrial membrane potential were observed by fluorescence intensity after mitochondria was extracted.Results: Sodium selenite suppressed the growth of SHG44 cells significantly,and statistical significance was found in 2.0 and 4.0μmol/L groups(P<0.05).Expression of ANT1 significantly increased in each selenium group(P<0.05).Mitochondrial membrane potential decreased significantly in 2.0 and 4.0μmol/L groups(P<0.05).Opening degree of mitochondrial permeability transition increased significantly in 1.0,2.0 and 4.0 μmol/L groups(P<0.05).Conclusion: Sodium selenite can suppress the SHG44 cell growth,and ANT1 may be involved in this mechanism,with decreasing mitochondrial membrane potential and increasing mitochondrial permeability transition opening degree.

关键词(KeyWords)： ANT1;亚硒酸钠;脑胶质瘤;△Ψm;MPTP
ANT1;sodium selenite;glioma;△Ψm;MPTP

Abstract:

Keywords:

基金项目(Foundation): 武警医学院科研基金面上项目(WYM201118);; 武警医学院科研基金博士启动金项目(WYB201110)

作者(Authors): 吕小生;陈旭义;汤锋武;张赛;蒋显锋;
LV Xiaoshen1,CHEN Xuyi2,TANG Fengwu2,ZHANG Shai2,JIANG Xianfeng2(1.Department of Cerebral Surgery,Leting County Hospital,Tangshan 063000,Hebei,China;2.Department of Cerebral Surgery,the Affiliated Hospital of Logistics Academy of the Armed Police Force,Dongli area 300162,Tianjin,China)

DOI: 10.19367/j.cnki.1000-2707.2012.06.016

参考文献(References)：

• [1]吕小生,陈旭义,汤锋武,等.亚硒酸钠对脑胶质瘤细胞生长及线粒体膜电位的影响[J].贵阳医学院学报,2012(2):127-131.
• [2]张杰,刘祯,景鹏,等.细胞线粒体膜电位的测量方法[J].首都医科大学学报,2006(1):124-125.
• [3]Clarke SJ,Mcstay GP,Halestrap AP.Sanglifehrin a actsas a potent inhibitor of the mitochondrial permeabilitytransition and reperfusion injury of the heart by binding tocyclophilin-D at a different site from cyclosporin A[J].JBiol Chem,2002(277):34793-34799.
• [4]Green DR,Kroemer G.The pathophysiology of mitochon-drial cell death[J].science,2004(5684):626-629.
• [5]Mohamad N,Gutierrez A,Nunez M,et al.mitochondrialapoptotic pathways[J].Biocell,2005(2):149-161.
• [6]Lucken-Ardjomande S,Martinou JC.Newcomers in theprocess of mitochondrial permeabilization[J].J Cell SCI,2005(Pt3):473-483.
• [7]Zamzami N,Hirsch T,Dallaporta B,et al.Mitochondrialimplication in accidental and programmed cell death:ap-optosis and necrosis[J].J Bioenerg Biomembr,1997(29):185-193.
• [8]Schubert A,Grimm S.Cyclophilin D,a component of thepermeability transition-pore,is anapoptosis repressor[J].Cancer Res,2004(1):85-93.

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