Inhibitory effects of a gradient static magnetic field on normal angiogenesis

✍ Scribed by Zhe Wang; Pengfei Yang; Huiyun Xu; Airong Qian; Lifang Hu; Peng Shang

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 264 KB
• Volume: 30
• Category: Article
• ISSN: 0197-8462
• DOI: 10.1002/bem.20501

✦ Synopsis

Abstract

Angiogenesis, the formation of new blood vessels, is critical in many normal and pathological processes such as development, reproduction, tumor growth, and metastasis. Recently, exposure to moderate‐intensity static magnetic fields (1 mT to 1 T) has attracted much attention for its potential therapeutic value as a noninvasive intervening method. Nevertheless, the effects of moderate‐intensity and spatial gradient static magnetic fields (GSMF) on angiogenesis have not received enough attention. In this study, the effects of GSMF (0.2–0.4 T, 2.09 T/m, 1–11 days) on angiogenesis were investigated both in vitro and in vivo. An MTT assay was used as an in vitro method to detect the proliferation ability of human umbilical veins endothelial cells (HUVECs). Two kinds of in vivo models, a chick chorioallantoic membrane (CAM) and a matrigel plug, were used to detect the effects of GSMF on angiogenesis. The results showed that the proliferation ability of HUVECs was significantly inhibited 24 h after the onset of exposure. With regard to the CAM model, vascular numbers in the CAM that was continuously exposed to the GSMF were all less than those in normal condition. In accordance with the gross appearance, the contents of hemoglobin in the models exposed to GSMF for 7–9 days were also less. In addition, similar to the CAM model, the results of vascular density and hemoglobin contents in the matrigel plug also demonstrated that the GSMF exposure for 7 or 11 days inhibited vascularization. These findings indicate that GSMF might inhibit or prevent new blood vessels formation and could be helpful for the treatment of some diseases relevant to pathological angiogenesis. Bioelectromagnetics 30:446–453, 2009. © 2009 Wiley‐Liss, Inc.