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低频脉冲电磁场对CRP作用下大鼠EPC增殖、凋亡及NO分泌的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2008年第4期
页码:
394-397
栏目:
基础研究
出版日期:
2008-08-20

文章信息/Info

Title:
Effects of low frequency pulsing electromagnetic fields on proliferation, apoptosis and NO secreting function of endothelial progenitor cells from rat bone marrow intervened by CRP
作者:
许旭东马彦卓韩凯赵小梅张荣庆李飞王海昌
第四军医大学西京医院心脏内科,陕西 西安 710032
Author(s):
XU Xudong MA Yanzhuo HAN Kai ZhAO Xiaomei ZHANG Rongqing LI Fei WANG Haichang
Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China
关键词:
低频脉冲电磁场内皮祖细胞C反应蛋白
Keywords:
low frequency pulsing electromagnetic fields endothelial progenitor cells Creactive protein
分类号:
R363
DOI:
-
文献标识码:
A
摘要:
目的 观察不同强度、不同作用时间的低频脉冲电磁场对C反应蛋白(CRP)作用下大鼠骨髓来源内皮祖细胞(EPC)增殖、凋亡及NO分泌能力的影响。方法 密度梯度离心法获得SD雄性大鼠的骨髓EPC,实验分为10组,即空白对照组、12 mg/L CRP组以及CRP+不同强度、不同作用时间(02 mT 2 h、4 h;06 mT 2 h、4 h;10 mT 2 h、4 h;14 mT 2 h、4 h)低频脉冲电磁场组。MTT法检测CPR对EPC增殖能力的影响,流式细胞仪检测CRP对EPC凋亡率的影响,硝酸还原酶法检测EPC培养液中NO含量的变化。结果 与空白对照组相比,12 mg/L CRP可明显抑制EPC增殖及NO分泌能力,促进EPC凋亡(P<005),06 mT 4 h;10 mT 2 h两组EPC增殖、NO分泌能力显著高于CRP组,EPC凋亡显著低于CRP组(P<005)。其余各组与CRP组相比无明显差异。结论 12 mg/L CRP可抑制EPC的增殖及NO分泌,促进其凋亡;06 mT 4 h和10 mT 2 h电磁场可拮抗CRP对EPC的作用,磁场对CRP环境下EPC的作用无强度及时间依赖性。
Abstract:
AIM To investigate effects of low frequency pulsing electromagnetic fields on the proliferation, apoptosis and NO secreting function of endothelial progenitor cells(EPCs)from bone marrow intervened by Creactive protein(CRP). METHODS EPCs were isolated from bone marrow blood of rat by density gradient centrifugation and were divided into ten groups: control group, 12 mg/L CRP group, and groups of CRP with 02 mT 2 h, 4 h;06 mT 2 h, 4 h;10 mT 2 h, 4 h;and 14 mT 2 h, 4 h. MTT assay was used to detect the effect of CRP on the multiplication ability of EPC and flow cytometry was used to detect the apoptosis caused by CRP. NO content was measured in the cell culture medium by nitrate reductase method. RESULTS CRP of 12 mg/L inhibited proliferation and NO secreting function and induced apoptosis of EPCs (P<005). In 06 mT 4 h group and 10 mT 2 h group, proliferation and NO secreting function of EPC was significantly higher than that in CRP group (P<005), whereas apoptosis of EPCs was significantly lower than that in CRP group (P<005). There was no difference in EPCs proliferation, apoptosis and NO secreting function between other groups and CRP group. CONCLUSION CRP of 16 mg/L inhibits proliferation and NO secreting function and induces apoptosis of EPCs. 06 mT 4 h and 10 mT 2 h of low frequency pulsing electromagnetic fields antagonize the effects of CRP on EPCs, increase the proliferation and NO secretion and decrease apoptosis of EPCs, with on intensitydependence.

参考文献/References

[1] Werner N, Nickenig G. Clinical and therapeutical implicationgs of EPC biology in atherosclerosis[J]. J Cell Mol Med, 2006, 10(2):318-332.

[2] Tepper OM, Callaghan MJ, Chang EI, et al. Electromagnetic fields increase in vitro and in vivo angiogenesis through endothelial release of FGF2\[J\]. FASEB J, 2004, 18(11):1231-1233.

[3] Verma S, Kuliszewski MA, Li SH, et al. Creactive protein attenuates endothelial progenitor cell survival, differentiation, and function: further evidence of a mechanistic link between Creactive protein and cardiovascular disease[J]. Circulation, 2004, 109(17):2058-2067.

[4] Ventura C, Maioli M, Asara Y, et al. Turning on stem cell cardiogenesis with extremely low frequency magnetic fields[J]. FASEB J, 2005, 19(1):155-157.

[5] Tepper OM, Capla JM, Galiano RD, et al. Adult vasculogenesis occurs through in situ recruitment, proliferation, and tubulization of circulating bone marrowderived cells[J]. Blood, 2005, 105(3):1068-1077.

备注/Memo

备注/Memo:
收稿日期:2007-10-29.基金项目:国家自然科学基金项目资助(30600580) 通讯作者:王海昌,主任医师,主要从事心律失常、冠心病的基础研究与介入治疗研究Email:wanghc@fmmu.edu.cn 作者简介:许旭东,硕士生Email:xuxdfmmu@sina.com
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