Department of Gerontology, Xin Hua Hospital, Shanghai Jiaotong University Kongjiang Road 1665, Shanghai 200092, China ; Department of Cardiology, Nagoya University Graduate School of Medicine 65 Tsuruma-cho, Showa-ku, Nagoya 466-8550, Japan.
Department of Gerontology, Xin Hua Hospital, Shanghai Jiaotong University Kongjiang Road 1665, Shanghai 200092, China ; Department of Cardiology, Hua Dong Hospital, Fudan University West Yan'an Road 221, Shanghai 200040, China.
Am J Transl Res. 2014 May 15;6(3):281-90. eCollection 2014.
Extracorporeal pulsed electromagnetic field (PEMF) has been shown the ability to improve regeneration in various ischemic episodes. Here, we examined whether PEMF therapy facilitate cardiac recovery in rat myocardial infarction (MI), and the cellular/molecular mechanisms underlying PEMF-related therapy was further investigated. The MI rats were exposed to active PEMF for 4 cycles per day (8 minutes/cycle, 30 ± 3 Hz, 5 mT) after MI induction. The data demonstrated that PEMF treatment significantly inhibited cardiac apoptosis and improved cardiac systolic function. Moreover, PEMF treatment increased capillary density, the levels of vascular endothelial growth factor (VEGF) and hypoxic inducible factor-1α in infarct border zone. Furthermore, the number and function of circulating endothelial progenitor cells were advanced in PEMF treating rats. In vitro, PEMF induced the degree of human umbilical venous endothelial cells tubulization and increased soluble pro-angiogenic factor secretion (VEGF and nitric oxide). In conclusion, PEMF therapy preserves cardiac systolic function, inhibits apoptosis and trigger postnatal neovascularization in ischemic myocardium.
体外脉冲电磁场（PEMF）已被证明具有改善各种缺血事件再生的能力。在这里，我们研究了 PEMF 治疗是否有助于大鼠心肌梗死（MI）的心脏恢复，以及进一步研究了与 PEMF 相关治疗相关的细胞/分子机制。MI 大鼠在 MI 诱导后每天接受主动 PEMF 治疗 4 个周期（8 分钟/周期，30 ± 3 Hz，5 mT）。数据表明，PEMF 治疗显著抑制心脏细胞凋亡并改善心脏收缩功能。此外，PEMF 治疗增加了梗塞边界区的毛细血管密度、血管内皮生长因子（VEGF）和缺氧诱导因子-1α的水平。此外，PEMF 治疗组循环内皮祖细胞的数量和功能得到了提高。在体外，PEMF 诱导人脐静脉内皮细胞的管腔形成程度，并增加可溶性促血管生成因子的分泌（VEGF 和一氧化氮）。总之，PEMF 治疗可维持心脏收缩功能，抑制细胞凋亡并触发缺血性心肌的后天血管新生。
