期刊文献+

氯化锂调节趋化因子Fractalkine表达抑制缺氧复氧诱导的血管内皮细胞损伤 被引量:1

The cytoprotective effects of Lithium chloride on HUVECs through regulating fractalkine during the anoxia/reoxygenation
下载PDF
导出
摘要 目的:观察缺氧复氧诱导人脐静脉血管内皮细胞(Human umbillcal vein endothelial cells,HUVECs)损伤和趋化因子(Fractalkine,FKN)表达变化及氯化锂(Lithium chloride,LiCl)的干预效应。方法:体外培养HUVECs并随机分为对照组、缺氧复氧组和LiCl 5、10 mmol/L组。MTT法测定HUVECs的存活率,流式细胞术检测HUVECs凋亡率,免疫细胞荧光技术检测HUVECs的FKN蛋白表达,RT-PCR技术检测HUVECs的FKN mRNA表达。结果:与对照组比较,缺氧复氧组HUVECs存活率显著降低但凋亡率显著增高(P<0.01)且FKN mRNA和蛋白质表达也显著增高(P<0.01);与缺氧复氧组比较,LiCl 5、10 mmol/L组HUVECs存活率显著增高但凋亡率显著降低(P<0.01)且FKNmRNA和蛋白质表达也明显降低(P<0.05)。结论:缺氧复氧上调FKN表达诱导HUVECs损伤(存活率降低、凋亡率增加);LiCl预处理能够下调FKN表达,显著减轻缺氧复氧导致的HUVECs损伤。 Objective:To investigate the cytoprotective effects of lithium chloride(LiCl) on human umbillcal vein endothelial cells(HUVECs) through regulating Fractalkine(FKN) during the anoxia/reoxygenation.Methods:HUVECs were cultivated and divided into four groups randomly(control group,anoxia/reoxygenation group,LiCl 5 mmol/L group,and LiCl 10 mmol/L group),which were used to establish the anoxia/reoxygenation models.The cell viability was detected by MTT method.The apoptosis rate of HUVECs was examined by Flow cytometry.The mRNA expression of FKN was assessed by RT-PCR.The intracellular distribution and expression of FKN were determined by immunofluorescent staining.Results:Compared with control group,the apoptotic rate of HUVECs increased but their viability rate reduced significantly in anoxia/reoxygenation group(all P0.01).The mRNA and protein expression of FKN were increased remarkably in anoxia/reoxygenation group compared to control group(P0.01).Compared with anoxia/reoxygenation group,the survival rate of HUVECs was increased but their apoptotic rate as well as the expression of FKN mRNA and FKN protein reduced significantly in LiCl 5 mmol/L and 10 mmol/L groups(P0.01 or P0.05).Conclusions:The anoxia/reoxygenation induced the damage of HUVECs through upregulating FKN expression.LiCl pretreatment can protect HUVECs against anoxia/reoxygenation injury via inhibiting FKN expression.
作者 殷菱 李法琦
出处 《重庆医科大学学报》 CAS CSCD 北大核心 2011年第7期818-821,共4页 Journal of Chongqing Medical University
关键词 缺氧复氧 内皮细胞 细胞凋亡 趋化因子 氯化锂 anoxia/reoxygenation endothelial cell apoptosis fractalkine lithium chloride
  • 相关文献

参考文献8

二级参考文献40

  • 1李建莎,吴人亮.糖原合成酶激酶3的调节与功能[J].医学分子生物学杂志,2006,3(5):383-386. 被引量:10
  • 2SCORRANO L. Caspase-8 goes cardiolipin: a new platform to provide mitochondria with microdomains of apoptotic signals? [J]. J Cell Biol, 2008, 183:579 -581.
  • 3FOURNIe G J, COURTIN J P, LAVAL F. Plasma DNA as a marker of cancerous cell death[J]. Cancer Lett, 1995, 91:221-227.
  • 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.

共引文献7

同被引文献8

  • 1Ryu J, Lee CW, Hong KH, et al. Activation of fracta-lkine/CX3CRl by vascular endothelial cells induces angio-genesis through VEGF-A/KDR and reverses hindlimb is-chaemia [J]. Cardiovasc Res, 2008,78:333 -340.
  • 2Bazan JF,Bacon KB,Hardiman G,et al. A new class ofmembrane-bound chemokine with a CX3C motif [ J] . Na-ture, 1997,385:640 - 644.
  • 3Imaizumi T, Yoshida H,Satoh K. Regulation of CX3CL1/fractalkine expression in endothelial cells [ J]. J Athero-scler Thromb, 2004, 11 :15 -21.
  • 4Manduteanu I, Pirvulescu M, Gan AM, et al. Similareffects of resistin and high glucose on P-selectin and fracta-lkine expression and monocyte adhesion in human endotheli-al cells [ J] . Biochem Biophys Res Commun, 2010,391 :1443 -1448.
  • 5Dobaczewski M,Xia Y,Bujak M, et al. CCR5 signalingsuppresses inflammation and reduces adverse remodeling ofthe infarcted heart, mediating recruitment of regulatory Tcells [J]. Am J Pathol, 2010,176:2177 -2187.
  • 6Auffray C, Fogg D, Garfa M, et al. Monitoring of bloodvessels and tissues by a population of monocytes with patrol-ling behavior [ J] . Science, 2007 , 317:666 -670.
  • 7高菡,李建强,张莉娟,赵卉.EPO对大鼠肺缺血再灌注损伤时FKN及MCP-1表达的影响[J].当代医学,2011,17(3):37-39. 被引量:3
  • 8武云娜,方敬爱,张晓东,孙艳艳,刘文媛.辛伐他汀对大鼠肾缺血再灌注损伤中Wnt/JNK影响的研究[J].中国中西医结合肾病杂志,2012,13(3):201-205. 被引量:2

引证文献1

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