期刊文献+

丹参多糖保护H_2O_2致心肌细胞损伤作用机制 被引量:11

The Protective Mechanism of Salvia Polysaccharides against Myocardial Cell Injury Induced by H_2O_2
下载PDF
导出
摘要 目的研究prohibitin在H2O2致心肌细胞氧化应激损伤中的表达及中药丹参多糖对其调节作用。方法以H2O2干预体外培养乳鼠心肌细胞建立氧化应激心肌损伤模型;MTT法检测细胞活力;流式细胞术检测细胞凋亡率;免疫印迹法检测prohibitin蛋白表达情况。结果与模型组相比,丹参多糖组的细胞活力明显上升,凋亡率显著降低,其中高剂量组尤为明显(P<0.01);prohibitin在正常心肌细胞内表达较低,而在模型组表达代偿性增高,丹参多糖用药组其表达有所增加,高剂量组增加更明显,与模型组相比有显著性差异(P<0.05)。结论丹参多糖可通过上调prohibitin蛋白表达发挥其保护H2O2致心肌细胞损伤的作用。 Objective To study the expression of prohibitin in oxidative stress myocardial cells induced by H2O2 and regulation of Salvia polysaccharides on it. Methods Use H2O2 to stimulate the primary cultured myocardial cells to establish cellular oxidative stress model;to check cell viability by MTT assay;flow cytometry was used to detect cell apoptosis;the expression of prohibitin was detected by western boltting. Results Compared with the model group,Salvia polysaccharide groups significantly increased cell viability and decreased the apoptosis ratio,especially the high dose group(P0.01);the expression of prohibitin was low in normal myocardial cells,while higher in the model group;SM polysaccharide treatment groups obviously increased its level,especially the high dose group;there was significantly difference compared with the model group(P0.05). Conclusion Salvia polysaccharides can protect myocardial cell injury induced by H2O2 by up-regulating the expression of prohibitin.
出处 《时珍国医国药》 CAS CSCD 北大核心 2011年第12期2889-2891,共3页 Lishizhen Medicine and Materia Medica Research
基金 国家自然科学基金(No.30572435 No.81072776) 广州市白云区科技项目(No.2010-kz-39)
关键词 氧化应激 丹参多糖 心肌细胞 凋亡 Oxidative stress Salvia polysaccharides Myocardial cells Apoptosis
  • 相关文献

参考文献10

  • 1Nijtmans L G, De J L,Artal S M, et al. Prohibitins act as a membrane - bound chaperone for the stabilization of mitochondrial proteins [ J ]. EMBO J,2000,19( 11 ) :2444. 被引量:1
  • 2Sharma A, Qadri A. Vi polysaccharide of Salmonella typhi targets the prohibitin family of molecules in intestinal epithelial cells and suppres- ses early inflammatory responses. [ J]. Proc Natl Acad Sci U S A ,2004, 101 (50) :17492. 被引量:1
  • 3Nijtmans L G, Artal S M, Grivell L A, et al. The mitochondrial PHB complex: roles in mitochondrial respiratory complex assembly, ageing and degenerative disease. [ J ]. Cell Mol Life Sci ,2002,59 (1) :143. 被引量:1
  • 4Battaglia, G. , Fan'ace MG, Mastroberardine PG, et al. Transglutaminase 2 ablation leads to defective function of mitochondrial respiratory com- plex I affecting neuronal vulnerability in experimental models of extra- pyramidal disorders [ J ], J Neurochem,2007,100 ( l ) :36. 被引量:1
  • 5任哲,钱令嘉,杨志华.氧化应激心肌细胞prohibitin表达与分布变化及其生物学意义[J].中国应用生理学杂志,2007,23(2):173-177. 被引量:5
  • 6Kim, N. , Lee Y, Kim H, et al. Potential biomarkers for ischemic heart damage identified in mitochondrial proteins by comparative proteomics [ J ]. Proteomics ,2006,6 (4) : 1237. 被引量:1
  • 7Liu XH, Ren Z,Zhan R, et al. Prohibitin protects against oxidative stress -induced cell injury in cultured neonatal cardiomyocyte [ J ]. Celt Stress Chaperones ,2009,14 ( 3 ) : 311. 被引量:1
  • 8Theiss, A. L. , Obertone TS, Merlin D, et al. , Interleukin - 6 transcrip- tionally regulates prohibitin expression in intestinal epithelial cells [ J ]. J Biol Chem,2007,282(17) :12804. 被引量:1
  • 9Wang S. , B. Zhang and D. V. Faller, BRG1/BRM and prohibitin are re- quired for growth suppression by estrogen antagonists [ J 1. EMBO J, 2004,23 ( 11 ) :2293. 被引量:1
  • 10Rajalingam, K. and T. Rudel, Ras -Raf signaling needs prohibitin [ J ]. Cell Cycle ,2005.4 ( 11 ) : 1503. 被引量:1

二级参考文献8

  • 1刘树森 魏影允.鼠肝线粒体内膜H-ATP酶ATP合成反应动力学[J].Acta Biochinica et Biophysica Sinica(生物化学与生物物理学报:英文版),1987,19(3):241-251. 被引量:10
  • 2Yang T S,Ou Yang T B,Yang J.The mechanicsm of free rasical injury of myocardial necrosis of Keshan disease[J].Adv Free Radic Biol Med,1991,1 (1):19-34. 被引量:1
  • 3Liu X H,Qian L J,Gong J B,et al.Proteomic analysis of mitochondrial proteins in caidiomyocytes from chronic stressed rat[J].Proteomics,2004,4 (10):3167-3176. 被引量:1
  • 4Steglich G,Neupert W,Langer T,et al.Prohibitins regulate membrane protein degration by the m-AAAprotease in mitochondria[J].Mol Cell Biol,1999,19 (5):3435-3442. 被引量:1
  • 5Nijtmans L G,De Jong L,Artal-Sanz M,et al.Prohibitins act as a membrane-bound chaperone for the stabilization of mitochondrial proteins[J].EMBO J,2000,19(11),2444-2451. 被引量:1
  • 6Halliwell B,Gutteridge J M,Free radicals in biology and medicine[M].2nd ed,Oxford:Clarendon Press,1989.1-105. 被引量:1
  • 7Gottlieb R A,Burleson K O,Kloner R A,et al.Reperfusion injury induces apoptosis in rabbit cardiomyocytes[J].J Clin Invest,1994,94(4):1621-1628. 被引量:1
  • 8宋学立,钱令嘉.氧化应激和心肌损伤[J].国外医学(卫生学分册),2000,27(1):30-32. 被引量:15

共引文献4

同被引文献154

引证文献11

二级引证文献83

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