期刊文献+

蛋白酶体抑制剂MG132对PC12细胞的增殖抑制作用 被引量:5

Inhibitory effect of proteasome inhibitor MG132 on PC12 cell proliferation
在线阅读 下载PDF
导出
摘要 目的:了解蛋白酶体抑制剂MG132对多巴胺能细胞PC12增殖和凋亡的影响.方法:用不同浓度的MG132处理PC12细胞3d,通过3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑溴盐(MTT)微量比色法检测MG132对PC12细胞增殖的影响,通过姬姆萨染色法和流式细胞术检测MG132对PC12细胞凋亡的影响.结果:在作用时间相同(3d)的条件下,随着MG132浓度的增高(0,1,2.5,5,10,20μmol/L),对PC12细胞增殖的抑制作用逐渐增强.当MG132浓度达到2.5μmol/L时,对PC12细胞的抑制率超过40%,IC50=3.78μmol/L.同时,MG132能够明显诱导PC12细胞凋亡:姬姆萨染色显示,浓度为2.5μmol/L的MG132作用3d,细胞凋亡率为24.7%,而对照为1.3%;流式细胞术分析结果表明,浓度为2.5μmol/L的MG132作用3d,细胞凋亡率为25.6%,而对照为0%.结论:蛋白酶体抑制剂MG132能够抑制多巴胺能细胞PC12的增殖并诱导细胞凋亡,蛋白酶体活性的丧失可能影响到多巴胺能细胞的生存. AIM: To investigate the effect of proteasome inhibitor MG132 on the proliferation and apoptosis of dopaminergic PC12 ceils. METHODS: PC12 ceils were treated with MG132 at different concentrations for 3 d. The effect of MG132 on the proliferation of PC12 cells was analyzed through MTT assay and the effect of MG132 on the apoptosis of PC12 ceils was analyzed through Giemsa staining and flow cytometry. RESULTS: Treated for a same period (3 d), the inhibitory effect of MG132 on PC12 ceil proliferation enhanced with the increment of the concentration of MG132(0, 1, 2.5, 5, 10, 20 μmot/L). The inhibitory rate exceeded 40% when the MG132 concentration was 2.5 μmot/L, and the 50% inhibiting concentration ( IC50 ) was 3.78 μmol/L. MG132 also induced the apoptosis of PC12 ceils obviously. The apoptosis index of the ceils treated by MG132 at 2.5 μmot/L for 3 d was 24.7% examined by Giemsa staining and 25.6% by flow cytometry, that of the control cells was 1.3% and 0% respectively. CONCLUSION: MG132 can inhibit the proliferation of dopaminergic PC12 ceils and lead to apoptosis. The disfunction of proteasome may do harm to the existence of dopaminergic ceils.
出处 《第四军医大学学报》 北大核心 2006年第12期1137-1139,共3页 Journal of the Fourth Military Medical University
基金 国家自然科学基金项目(30471434)
关键词 蛋白酶体抑制剂 PC12细胞 帕金森病 细胞凋亡 proteasome inhibitor PC12 ceils Parkinson disease apoptosis
  • 相关文献

参考文献7

二级参考文献9

  • 1[1]Beal MF. Experimental models of Parkinson's disease [J]. Nat Rev Neurosci, 2001; 2(5): 325-334.
  • 2[2]Eberling JL, Jagust WJ, Taylor S, et al. A novel MPTP primate model of Parkinson's disease: Neurochemical and clinical changes [J]. Brain Res, 1998; 805(1-2): 259-262.
  • 3[3]Emborg ME, Tetrud JW, Moirano J, et al. Rest tremor in rhesus monkeys with MPTP-induced parkinsonism [J]. Front Biosci, 2003; 8: 148-154.
  • 4[4]Wichmann T, DeLong MR. Pathophysiology of Parkinson's disease: The MPTP primate model of the human disorder [review] [J]. Ann N Y Acad Sci, 2003; 991: 199-213.
  • 5[5]Warner TT, Schapira AH. Genetic and environmental factors in the cause of Parkinson's disease [J]. Ann Neurol, 2003; 53(Suppl 3): S16-25.
  • 6[6]Pollack AE. Anatomy, physiology, and pharmacology of the basal ganglia [J]. Neurol Clin, 2001; 19(3): 523-534.
  • 7[8]Cohen-Cory S. The developing synapse: Construction and modulation of synaptic structures and circuits [J]. Science, 2002; 298(5594): 770-776.
  • 8[10]Martinez M, Hernandez AI, Martinez N. N-Acetylcysteine delays age-associated memory impairment in mice: Role in synaptic mitochondria [J]. Brain Res, 2000; 855(1): 100-106.
  • 9林宏,宿长军.经颅重复低频磁刺激后大鼠苍白球和黑质酪氨酸羟化酶阳性标记变化[J].第四军医大学学报,2001,22(15):1384-1387. 被引量:2

共引文献11

同被引文献54

引证文献5

二级引证文献7

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部