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氯化锂对大鼠缺血再灌注损伤心肌细胞凋亡的影响 被引量:3

Lithium chloride modulates myocardial apoptosis in rat with myocardial ischemia reperfusion injury
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摘要 目的:研究大鼠心肌缺血再灌注损伤心肌凋亡以及氯化锂的干预作用。方法:健康SD大鼠随机分4组:①正常对照组(A组,5只),②心肌缺血再灌注组(B组,15只),③心肌缺血再灌注+0.9%氯化钠组(C组,15只),④心肌缺血再灌注+氯化锂组(D组,15只),B,C,D组又分为1h、3h、6h3个亚组,每个亚组5只大鼠。流式细胞仪检测心肌细胞凋亡率,RT-PCR和WesternBlot分别检测凋亡相关基因蛋白Bcl-2和Caspase-3的表达。结果:与A组比较,B、C组3h心肌细胞凋亡率增高、Bcl-2减少、Casepase-3增多,差异有统计学意义;D组心肌细胞凋亡率下降、Bcl-2和Casepase-3表达与A组差异无统计学意义。结论:心肌再灌注损伤引起心肌细胞凋亡增多,Bcl-2降低以及Caspase-3增高,氯化锂能够减轻以上变化。 Objective: To study the effects of lithium chloride on apoptosis and the related proteins of myocardial cells in the rats with myocardial isehemia reperfusion injury. Method: SD rats were divided randomly into 4 groups: (1)normal control group(group A, n=5), (2)myocardial ischemia reperfusion (MIR) group(group B, n= 15), (3)MIR+Saline group(group C, n= 15), (4)MIR+lithium chloride group(group D, n= 15). The B, C and D group were divided into 1 h, 3 h and 6 h subgroups with 5 rats in each subgroup. Flow cytometry was used to detecte the cadiocyte apoptosis rate. Apoptosis-related proteins Bcl-2, Caspase-3 were detected by the methods of RT-PCR and Western-blot. Result: Compared with group A, the cadiocyte apoptosis rate increased, Bcl-2 reduced, Casepase-3 increased significantly at 3 hours in group B and C. Whereas the cadiocyte apoptosis rate decreased in group D, and the expression of Bal-2 and Casepase-3 reached back to group A. Conclusion: Myocardial ischemia reperfusion injury induces increase of myocardial cell apoptosis, decrease of Bcl-2 and increase of Caspase- 3. Lithium chloride can relief above changes, suggesting that lithium chloride has protective effects against myocardial isehemia reperfusion injury.
出处 《临床心血管病杂志》 CAS CSCD 北大核心 2009年第6期468-471,共4页 Journal of Clinical Cardiology
关键词 心肌缺血再灌注损伤 凋亡 BCL-2 CASPASE-3 氯化锂 myocardial ischemia reperfusion injury apoptosis Bcl-2 Caspase-3 lithium chloride
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参考文献10

  • 1SCORRANO L. Caspase-8 goes cardiolipin: a new platform to provide mitochondria with microdomains of apoptotic signals? [J]. J Cell Biol, 2008, 183:579 -581.
  • 2FOURNIe G J, COURTIN J P, LAVAL F. Plasma DNA as a marker of cancerous cell death[J]. Cancer Lett, 1995, 91:221-227.
  • 3刘先义,邹捍东,余金甫,黄海波,熊桂仙.参附注射液对缺血再灌注家兔多脏器损伤的治疗作用[J].中华麻醉学杂志,1997,17(7):430-432. 被引量:94
  • 4EPPINGER M J, DEEB G M, BOLLING S F. Mediators of ischemia-reperfusion injury of rat lung[J].Am J Pathol, 1997, 150:1773- 1784.
  • 5LIN Y T, YANG J S, LIN S Y. Diallyl disulfide (DADS) induces apoptosis in human cervical cancer Ca Ski cells via reactive oxygen species and Ca2+-dependent mitochondria-dependent pathway[J]. Anticancer Res, 2008, 28:2791-2799.
  • 6VOUTSADAKIS I A. Apop tosis and the pathogenesis of lymphoma [J]. Acta Oncol, 2000, 39:151- 156.
  • 7WALTER D, SCHMICH K, VOGEL S. Switch from type II to I Fas/CD95 death signaling on in vitro culturing of primary hepatocytes[J].Hepatology, 2008, 48:1942-1953.
  • 8CYR L, LANGLER R, LAVIGNE C. Cell cycle arrest and apoptosis responses of human breast epitheli- al cells to the synthetic organosulfur compound p me thoxyphenyl p-toluenesulfonate[J]. Anticaneer Res, 2008, 28:2753 -2763.
  • 9NISHIKAWA T, TSUNO N H, TSUCHIYA T. Sulforaphane stimulates activation of proapoptotic protein hax leading to apoptosis of endothelial progenitor cells[J].Ann Surg Oncol, 2009, 16: 534-543.
  • 10MANCEUR A P, DRISCOLL B D, SUN W, et al. Selective enhancement of the uptake and bioactivity of a TAT-conjugated peptide inhibitor of glycogen synthase kinase-3[J]. MolTher, 2009, 17:500-507.

二级参考文献9

  • 1彭毅志,中国急救医学,1996年,1期,53页
  • 2罗巍,中国危重病急救医学,1995年,7卷,68页
  • 3程亚明,中华创伤杂志,1995年,11卷,53页
  • 4韦文哲,河北医药,1993年,1期,1页
  • 5王左,中国中医急症,1993年,2卷,173页
  • 6张世玮,江苏中医杂志,1990年,2卷,43页
  • 7丁培林,中医杂志,1988年,29卷,24页
  • 8贾红慧,中成药,1983年,15卷,35页
  • 9吴葆杰,中草药药理学,1983年,46页

共引文献93

同被引文献29

  • 1周舟,余晓东,张蕾,李茂全,张广斌,余争平.GSK3β激活参与缺氧诱导心肌细胞凋亡[J].第三军医大学学报,2006,28(17):1738-1741. 被引量:3
  • 2Boudina S, Abel ED. Diabetic eardiomyopathy revisited [J]. Circulation, 2007, 115 (25) : 3213-3223.
  • 3Williams R, Ryves WJ, Dalton EC, et al. A molecular cell biology of lithium [ J ]. Biochem Soc Trans, 2004, 32 (Pt5): 799-802.
  • 4Harrell NB, Teachey MK, Gifford NJ, et al. Essential role of p38 MAPK for activation of skeletal muscle glucose transport by lithium [J]. Arch Physiol Biochem, 2007, 113 (4): 221-227.
  • 5Maneeur AP, Driscoll BD, Sun W, et al. Selective enhancement of the uptake and bioaetivity of a TAT- conjugated peptide inhibitor of glycogen synthase kinase-3 [J]. Mol Ther, 2009, 17 (3):500-507.
  • 6SchannwelI CM, Schneppenheim M, Perings S, et al. Left ventricular diastolic dysfunction as an early manifestation of diabetic cardiomyopathy [J]. Cardiology, 2002, 98 (1/2): 33-39.
  • 7Li F, Chong ZZ, Maiese K. Winding through the WNT pathway during cellular development and demise [J]. Histol Histopathol, 2006, 21 (1): 103-124.
  • 8Osakada F, Takahashi M. Drug development targeting the glycogen synthase kinase-3beta (GSK-3beta) -mediated signal transduction pathway: targeting the Wnt pathway and transplantation therapy as strategies for retinal repair [J]. J Pharmacol Sci, 2009, 109 (2): 168-173.
  • 9Hirotani S, Zhai P, Tomita H, et al. Inhibition of glycogen synthase kinase 3beta during heart failure is protective [J]. Circ Res, 2007, 101 (11): 1164-1174.
  • 10Oomez L, Paillard M, Thibauh H, et al. Inhibition of GSK3beta by postconditioning is required to prevent opening of the mitochondrial permeability transition pore during reperfusion [J]. Circulation, 2008, 117 (21) : 2761-2768.

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