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亚硒酸钠对脑胶质瘤细胞生长及线粒体膜电位的影响 被引量:1

Inhibitory Effect of Sodium Selenite on the Growth of Human Glioma Cell and Its Effect on Mitochondrial Membrane Potential
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摘要 目的:研究亚硒酸钠对人脑胶质瘤细胞生长抑制效应及线粒体膜电位的影响。方法:使用不同浓度的亚硒酸钠(0.004、0.020、0.100及0.500μmol/L)对人脑胶质瘤细胞SHG-44进行侵染,通过四甲基偶氮唑盐(MTT)比色法检测亚硒酸钠对SHG-44增殖的影响,提取细胞线粒体后通过激光扫描共聚焦显微镜下观察SHG-44的荧光强度,分析SHG-44的线粒体膜电位。结果:亚硒酸钠对人脑胶质瘤细胞生长具有明显的抑制作用,且随亚硒酸钠浓度的增加抑制作用逐渐加强,0.100及0.500μmol/L染硒组与对照组相比差异均有统计学意义(P<0.05),0.004及0.020μmol/L染硒组与对照组相比差异无统计学意义(P>0.05);0.100、0.500μmol/L染硒组线粒体膜电位显著降低(P<0.05),0.004及0.020μmol/L组与对照组相比差异无统计学意义(P>0.05)。结论:亚硒酸钠能抑制人脑胶质瘤细胞SHG-44生长,并且降低其线粒体膜电位。 Objective: To investigate the inhibitory effects of sodium selenite on the growth of human glioma cell SHG-44 and its effect on mitochondrial membrane potential.Methods: SHG-44 cells were treated with different concentrations(0.004 μmol/L,0.020 μmol/L,0.100 μmol/L,0.500 μmol/L)of sodium selenite.The effect of sodium selenite on proliferation of SHG-44 cells was detected by MTT assay.The mitochondria was extracted,and fluorescence intensity of SHG-44 cells were detected under laser scanning confocal microscopy,and mitochondrial membrane potential of SHG-44 cells was analyzed.Results: Sodium selenite significantly suppressed the growth of SHG-44 cells.The cell growth rate decreased with the concertration increase of sodium selenite.Statistical differences were found between 0.100 μmol/L,0.500 μmol/L groups and control group(P0.05),but not between 0.004 μmol/L,0.020 μmol/L groups and control group(P0.05).Mitochondrial membrane potential was decreased significantly in 0.100 and 0.500 μmol/L groups(P0.05),but not in 0.004 μmol/L and 0.020 μmol/L groups(P0.05).Conclusions: Sodium selenite can suppress the SHG-44 cell growth,and down-regulate the mitochondrial membrane potential.
出处 《贵阳医学院学报》 CAS 2012年第2期167-169,共3页 Journal of Guiyang Medical College
基金 武警后勤学院科研基金面上项目(WYM201118)
关键词 亚硒酸钠 神经胶质瘤 细胞 线粒体 膜电位 sodium selenite glioma cells mitochondria membrane potentials
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参考文献8

  • 1Clark LC,Combs GF,Turnbull BW,et al.Effects of sele-nium supplementation for cancer prevention in patientswith carcinoma of the skin[J].A randomized controlledtrial.Nutritional Prevention of Cancer Study Group.JA-MA,1996(24):1957-1963.
  • 2张杰,刘祯,景鹏,李国君.细胞线粒体膜电位的测量方法[J].首都医科大学学报,2006,27(1):124-125. 被引量:13
  • 3俸家富,李少林.硒硒蛋白和硒的抗癌机理[J].微量元素与健康研究,2001,18(1):70-72. 被引量:21
  • 4刘静颖,王海帆,赏诗樟.亚硒酸钠对移植于裸鼠人神经胶质瘤的生长抑制作用[J].临床与实验病理学杂志,1992,8(A08):56-58. 被引量:1
  • 5Nève J.Human selenium supplementation as assessed bychanges in blood selenium concentration and glutathioneperoxidase activity[J].J Trace Elem Med Biol,1995(2):65-73.
  • 6Seko Y,Satito Y,Kitabara J.Selenium in biology andmedicine[M].Berlin:Springer-Verlag,1989:70-73.
  • 7Mohamad N,Gutierrez A,Nunez M,et al.Mitochondrialapoptotic pathways[J].Biocell.2005(2):149-161.
  • 8Lucken-Ardjomande S, Martinou JC. Newcomers in the process of mitochondrial penneabilization[J]. J Cell SCI, 2005 (3) : 473 - 483.

二级参考文献17

  • 1[1]Gladyshev VN,Jeang K,Wootton JC,et al. A new human selenium containingg protein. J. Biol. Chem, 1998,273:8910~8915
  • 2[2]Ip C,Thompson HJ,Zhu Z,et al. In vitro and in vivo studies of methylseleninic acid: evidence that a monomathylated selenium mataboliteis critical for cancer chem oprevention. Cancer Res , 2000,60: 2882 ~ 6
  • 3[3]Andreadou I,Water B,Commander JNM,et al. Comparative cytotoxicity of 14 novel selenocysteine Se- conjugates in rat renal proximal tubular cells. Toxicol. Apk.Pharmacok, 1996,141: 278~287
  • 4[4]Kaeca ML,Lu J,Strange R,et al. Differential indruction of growth arrest inducible genes by selenium compounds. Biochem. Pharmacol, 1997,53: 921-926
  • 5[5]Sinha R,Medina D. Inhibition of cdk2 kinase activity by methylselenocysteine in synchronized mouse mammaryepithelial tumor cells. Carcinogenesis, 1997, 18:1541 ~1547
  • 6[6]Howard EG. Selenium metabolism, selenoproteins and mechanisms of cancer prevention: complexities with thioredoxin reductase. Carcinogenesis, 1999,20: 1657 ~1666
  • 7[7]Gopalakrishna R, Gundimeda U, Chen SH. Cancer- preventive selenocompounds induce a specific redox modification of cysteine- rich regions in Ca2+- dependent isozymes of protein kinase C. Arch. Biochem. Biophys,1997,348:25~36
  • 8[8]Kim IY,Stadtman TC. Inhibiton of NF-kB DNA binding and nitric oxide induction in human Tcells and lung adenocarcinoma cells by selenite treatment. Proc. Natl.Acad. Sci. USA, 1997,94:12904~12907
  • 9[9]Mustacich D,Powis G. Throredoxin reductase. Bichem J.2000,15: 346
  • 10[10]Gladyshev VN,Sun QA,Wu YL,et al. Redox regulation of cell signaling by selenocysteine in mammalian thioredoxin reductases. FASEB J, 1999,13 :A1579

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同被引文献7

  • 1张杰,刘祯,景鹏,李国君.细胞线粒体膜电位的测量方法[J].首都医科大学学报,2006,27(1):124-125. 被引量:13
  • 2Clarke SJ, Mcstay GP, Halestrap AP. Sanglifehrin a acts as a potent inhibitor of the mitochondrial permeability transition and reperfusion injury of the heart by binding to cyclophilin-D at a different site from cyclosporin A[ J ]. J Biol Chem, 2002(277) :34793 - 34799.
  • 3Green DR, Kroemer G. The pathophysiology of mitochon- drial cell death [ J ]. science, 2004 (5684) : 626 - 629.
  • 4Mohamad N, Gutierrez A, Nunez M, et al. mitochondrial apoptotic pathways [ J ]. Biocell, 2005 ( 2 ) : 149 - 161.
  • 5Lucken-Ardjomande S, Martinou JC. Newcomers in the process of mitochondrial permeabilization [ J ]. J Cell SCI, 2005 ( Pt3 ) : 473 - 483.
  • 6Zamzami N, Hirsch T, Dallaporta B, et al. Mitochondrial implication in accidental and programmed cell death: ap- optosis and necrosis [ J ]. J Bioenerg Biomembr, 1997 (29) :185 - 193.
  • 7Schubert A, Grimm S. Cyclophilin D, a component of the permeability transition-pore, is anapoptosis repressor[ J]. Cancer Res, 2004( 1 ) :85 -93.

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