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P53在高糖诱导心肌细胞凋亡中的作用 被引量:2

Role of P53 in high glucose-induced apoptosis of cardiac muscle cells
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摘要 目的探讨P53在高糖诱导心肌细胞凋亡中的作用。方法将培养的SD大鼠乳鼠心肌细胞随机分为4组:对照组、P53抑制剂组(葡萄糖浓度为5.5mmol/L,P53抑制剂浓度为50μmol/L)、高糖组(葡萄糖浓度为25mmol/L)和高糖+P53抑制剂组(P53抑制剂浓度为50μmol/L)。噻唑盐比色法(MTT法)检测心肌细胞活性,流式细胞术检测细胞凋亡,Western blot对各组细胞P53、BAX和Caspase-3进行半定量分析。结果与对照组相比,高糖组心肌细胞活力明显降低,凋亡率明显升高,Caspase-3、BAX和线粒体蛋白P53表达增多。与P53抑制剂组相比,高糖组心肌细胞活力明显降低,凋亡率明显升高,Caspase-3、BAX和线粒体蛋白P53表达增多;高糖+P53抑制剂组心肌细胞活力也有所降低,凋亡率升高,Caspase-3、BAX和线粒体蛋白P53表达增多。与高糖组相比,高糖+P53抑制剂组的心肌细胞活力增高,凋亡率明显降低,Caspase-3、BAX和线粒体蛋白P53表达减少。结论高糖可能通过介导P53转位到线粒体激活凋亡通路,引起心肌细胞凋亡。 Objective To study the role of P53 in high glucose-induced apoptosis of cardiac muscle cells.Methods Cardiac muscle cells from SD rats were cultured and randomly divided into control group,P53 inhibitor(pifithrin-α) group(with a glucose concentration of 5.5mmol/L and a concentration of 50μmol/L),high glucose(25mmol/L) group,and high+ pifithrinα(50μmol/L) group.Viability and apoptosis of cardiac muscle cells were detected by MTT assay and flow cytometry,respectively.Expression levels of P53,Bax and caspase-3 in cardiac muscle cells were measured by Western blot.Results The viability of cardiac muscle cells was significantly lower,the apoptosis rate of cardiac muscle cells was significantly higher,and the expression levels of P53,Bax and caspase-3 in cardiac muscle cells were significantly higher in high glucose group and high+ pifithrin-α group than in control group and P53 inhibitor group(P0.05).The viability of cardiac muscle cells was significantly higher,the apoptosis rate of cardiac muscle cells was significantly lower,and the expression levels of P53,Bax and caspase-3 in cardiac muscle cells were significantly lower in high glucose + pifithrin-α group than in high glucose group(P0.05).Conclusion High glucose can induce apoptosis of cardiac muscle cells by mediating transposition of P53 to mitochondria-activated apoptosis pathway.
出处 《军医进修学院学报》 CAS 2012年第3期269-272,共4页 Academic Journal of Pla Postgraduate Medical School
基金 博士科研启动基金项目(No.20091050)
关键词 高糖 P53 心肌细胞 high glucose P53 cardiomyocytes
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参考文献8

  • 1Kumar SD,Dheen ST,Tay SS.Maternal diabetes induces congenitalheart defects in mice by altering the expression of genes involved incardiovascular development[J].Cardiovasc Diabetol,2007,6:34.
  • 2Bergner DW,Goldberger JJ.Diabetes mellitus and sudden cardiacdeath:what are the data?[J].Cardiol J,2010,17(2):117-129.
  • 3Aharinejad S,Andrukhova O,Lucas T,et al.Programmed celldeath in idiopathic dilated cardiomyopathy is mediated by suppressionof the apoptosis inhibitor Apollon[J].Ann Thorac Surg,2008,86(1):109-114.
  • 4Dallak MM,Mikhailidis DP,Haidara MA,et al.Oxidative stress asa common mediator for apoptosis induced-cardiac damage in diabeticrats[J].Open Cardiovasc Med J,2008,2:70-78.
  • 5Pietsch EC,Sykes SM,Mcmahon SB,et al.The p53 family andprogrammed cell death[J].Oncogene,2008,27(50):6507-6521.
  • 6Caelles C,Helmberg A,Karin M.p53-dependent apoptosis inthe absence of transcriptional activation of p53-target genes[J].Nature,1994,370(6486):220-223.
  • 7Endo H,Saito A,Chan PH.Mitochondrial translocation of p53underlies the selective death of hippocampal CA1 neurons after globalcerebral ischaemia[J].Biochem Soc Trans,2006,34(Pt 6):1283-1286.
  • 8Cohn GM.Caspase:the executioners of apoptosis[J].Biochem J,1997,326(Pt1):1-16.

同被引文献21

  • 1屈朝法,马礼坤,徐少东,吴学平.急性心肌梗死晚期再灌注后心肌细胞凋亡与Bcl-2、Bax蛋白表达的研究[J].中国病理生理杂志,2007,23(4):656-659. 被引量:17
  • 2Bergner D W,Goldberger J J. Diabetes mellitus and sudden cardiac death:what are the data?[J]. Cardiol J ,2010,17(2) : 117-- 129.
  • 3Sun J,Xu Y,Dai Z,et al. Intermittent high glucose enhances prolif- eration of vascular smooth muscle cells by upregulating osteopontin [J]. Mol Cell Endocrinol,2009,313(1/2):64--69.
  • 4Yang L B,Qi W B, Lv X H,et al. Intermittent high glucose pro- motes expression of proinflammatory cytokines in monocytes[J]. InflammRes,2011,60(4):367 370.
  • 5Chen G,Chen Y,Chen H, et al. The effect of NF-~B pathway on proliferation and apoptosis of human umbilical vein endothelial cells induced by intermittent high glucose[J]. Mol Cell Bioehem, 2011, 347(1/2) :127--133.
  • 6Cole M P, Tangpong J, Oberley T D, et al. Nuclear interaction be- tween ADR induced p65 and p53 mediates cardiac injury in iNOS (-/-) mice[J]. PLoS One,2014,9(2) :e89251.
  • 7Leung A A,Eurich D T,Lamb D A,et al. Risk of heart failure in patients with recent-onset type 2 diabetes: population-based cohort study[J].J Card Fail,2009,15(2) : 152-- 157.
  • 8Ho F M,Lin W W,Chen B C,et al. High glucose-induced apoptosis in human vascular endothelial ceils is mediated through NF-kappa B and c-Jun NH2-terminal kinasc pathway and prevented by PI3K/ Akt/eNOS pathway[J].Cell Signal, 2006,18 (3): 391 -- 399.
  • 9Oeckinghaus A, Hayden M S, Ghosh S, et al. Crosstalk in NF-~B signaling pathways[J]. Nat Immunol,2011,12(8):695--708.
  • 10Wang F,Li H,Shi H, et al. Pro-apoptotic role of nuclear factor-~B in adriamycin-induced acute myocardial injury in rats[J]. Mol Med Rep,2012,5(2) :400--404.

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