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依达拉奉对硝普钠诱导的PC12细胞凋亡的保护作用

The Effects of Edaravone on the Apoptosis in PC12 Cells Induced by Sodium Nitroprusside
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摘要 目的:探讨依达拉奉对硝普钠诱导的PC12细胞凋亡的影响。方法:体外培养PC12细胞,并分为依达拉奉对硝普钠保护组(含500μmol/L硝普钠和75μmol/L依达拉奉)、硝普钠诱导组(含500μmol/L硝普钠)和对照组。采用MTT法检测细胞的增殖率;流式细胞术检测细胞的凋亡情况;Western-blot检测凋亡抑制蛋白Bcl-2和凋亡促进蛋白Bad的表达。结果:与对照组相比,硝普钠处理的PC12细胞增殖率显著降低,而细胞凋亡率显著升高,细胞内Bcl-2的表达显著减少,而Bad的表显著增加,差异均具有统计学意义(P<0.05);与单纯硝普钠诱导组相比,依达拉奉处理组细的胞增殖率显著增加而细胞凋亡率显著减少,同时Bcl-2的表达显著增加,而Bad的表达明显减少,差异均具有统计学意义(P<0.05)。结论:依达拉奉对硝普钠诱导的PC12细胞凋亡具有抑制作用,可能通过增加Bcl-2的表达并降低Bad的表达发挥抗凋亡作用。 Objective:To investigate the effect of edaravone on the apoptosis in PC12 cells induced by sodium nitroprusside. Methods: PC12 cells were cultured in vitro and divided into three groups: the control group, sodium nitropmsside (SNP) group and edaravone (EDA) group. The proliferation of PC12 was measured by thiazolyl blue (MTT) assay. The cell apoptosis was determined by Annexin V-FITC flow cytometry. Western blotting was performed to detect the protein expression of Bad and Bcl-2. Results: Compared with the control group, the proliferation decreased and the apoptosis increased in PC 12 cells induced by sodium nitroprusside, the protein expression of Bcl-2 decreased and the protein expression of Bad increased significantly (P〈0.05). Compared with SNP, EDA promoted the proliferation and inhibited the apoptosis in PC12. The expression of Bcl-2 increased and Bad decreased significantly after being treated with EDA in PCI2 (P〈0.05). Conclusion: Edaravone could inhibit the apoptosis in PC12 cells induced by sodium nitroprusside, the decreased expression of Bad and increased expression of Bcl-2 may be involved in the anti-apoptosis of Edaravone.
出处 《现代生物医学进展》 CAS 2013年第35期6900-6903,共4页 Progress in Modern Biomedicine
关键词 依达拉奉 PC12 凋亡 硝普钠 BCL-2 BAD Edaravone PC12 Apoptosis Sodium nitroprusside Bcl-2 Bad
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参考文献15

  • 1Schaller B,GrafR. Cerebral ischernia and reperfusion; the pathophysiologic concept as a basis for clinical theraphy[J].Journal of Cerebral Blood Flow and Metabolism,2004.351-371.
  • 2Charriaut MC,Remolleau S,Aggoun ZD. Apoptosis and programmde cell death:a role in cerebral ischemia[J].Biomedicine and Pharmacotherapy,1998.264-269.
  • 3Chen XW,Ashfaq S. Neuroprotective effects of free radical scavengers in stroke[J].Drugs & aging,2007,(07):537-546.
  • 4Chen H,Wang S,Ding JH. Edaravone protects against MPP+-induced cytotoxicity in rat primary cultured astrocytes via inhibition ofmitochondrial apoptotic pathway[J].Journal of Neurochemistry,2008.2345-2352.
  • 5WenJ,WatanabeK,MaM. Edaravone Inhibits JNK-c-Jun Pathway and Restores Anti-oxidative Defense after Ischemia-Reperfusion Injury in Aged Rats[J].Biological and Pharmaceutical Bulletin,2006,(04):713-718.doi:10.1248/bpb.29.713.
  • 6吉海杰,周蕾,陈乃宏.依达拉奉对硝普钠诱导PC12细胞氧化应激的保护作用[J].中国药理学通报,2011,27(9):1201-1204. 被引量:7
  • 7Wade SS. Pathophysiology of fecal cerebral ischemia:a therapeutic erspective[J].J Vasc Inlerv Radiol,2004.S3-S12.
  • 8Kawasaki T,Ishihara K,Ago Y. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one),a radical scavenger,prevents 1-meth-yl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicityin the substantia nigra but not the striatum[J].Journal of Pharmacology and Experimental Therapeutics,2007,(01):274-281.
  • 9Yoshida H,Kwon AH,Kaibori M. Edaravone prevents iNOS expression by inhibiting its promoter transactivation and mRNA stability in cytokine-stimulated hepatocytes[J].Nitric Oxide,2008.105-112.
  • 10盛钰,吴韶梅,赵欣.依达拉奉对硝普钠诱导PC12细胞氧化应激的影响分析[J].北方药学,2011,8(9):42-42. 被引量:1

二级参考文献42

  • 1Oechmichen M, Meissner C. Cerebral hypoxia and ischemia: the forensic point of view: a review. J Forensic Sci 2006, 51: 880- 887.
  • 2Won S J, Kim DY, Gwag BJ. Cellular and molecular pathways of ischemic neuronal death. J Biochem Mol Biol 2002, 35: 67-86.
  • 3Li RC, Morris MW, Lee SK, Pouranfar F, Wang Y, Gozal D. Neuroglobin protects PC12 cells against oxidative stress. Brain Res 2008, 1190: 159-166.
  • 4Thornberry NA, Rano TA, Peterson EP, Rasper DM, Timkey T, Garcia-Calvo M, et al. A combinatorial approach defines specificities of members of the caspase family and granzyme B. Functional relationships established for key mediators of apoptosis. J Biol Chem 1997, 272: 17907-17911.
  • 5Walford GA, Moussignac RL, Scribner AW, Loscalzo J, Leopold JA. Hypoxia potentiates nitric oxide-mediated apoptosis in endothelial cells via peroxynitrite-induced activation of mitochondria-dependent and -independent pathways. J Biol Chem 2004, 279: 4425-4432.
  • 6Li P, Nijhawan D, Budihardjo I, Srinivasula SM, Ahmad M, Alnemri ES, et al. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. Cell 1997, 91: 479-489.
  • 7Araya R, Uehara T, Nomura Y. Hypoxia induces apoptosis in human neuroblastoma SK-N-MC cells by caspase activation accompanying cytochrome c release from mitochondria. FEBS Lett 1998, 439: 168-172.
  • 8Sandner P, Wolf K, Bergmaier U, Gess B, Kurtz A. Hypoxia and cobalt stimulate vascular endothelial growth factor receptor gene expression in rats. Pflugers Arch 1997, 433: 803-808.
  • 9Zou W, Yan M, Xu W, Huo H, Sun L, Zheng Z, et al. Cobalt chloride induces PC12 cells apoptosis through reactive oxygen species and accompanied by AP-1 activation. J Neurosci Res 2001, 64: 646-653.
  • 10Jung JY, Kim WJ. Involvement of mitochondrial- and Fas-mediated dual mechanism in CoCl2-induced apoptosis of rat PC12 cells. Neurosci Lett 2004, 371: 85-90.

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