Song Xueqin, Zhang Ya, Hou Zhigang, Wu Hongran, Lu Shan, Tang Jin, Chen Xuexiao, Cui Hongying, Li Yuan, Bi Yue, Duan Weisong, Li Zhongyao, Li Chunyan
Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China.
Institute of Cardiocerebrovascular Disease, Shijiazhuang, Hebei 050000, P.R. China.
Exp Ther Med. 2018 Feb;15(2):1825-1830. doi: 10.3892/etm.2017.5610. Epub 2017 Dec 11.
Duchenne muscular dystrophy (DMD) is a fatal neuromuscular disease caused by the absence of dystrophin. Vascular endothelial growth factor (VEGF) is a heparin-binding dimeric glycoprotein and principal angiogenic factor stimulating the migration, proliferation and expression of various genes in endothelial cells. Recently, VEGF was demonstrated to exhibit an antiapoptotic and direct myogenic effect, as well as to enhance muscle force restoration subsequent to traumatic injury. Therefore, the present study attempted to assess the muscle damage of VEGF overexpression in mdx mice. Adeno-associated virus serotype 9 (AAV9)-VEGF was administered intravenously to mdx mice. At 4 weeks after injection, VEGF was observed to be upregulated in the tibialis anterior muscle. In addition, the serum creatine kinase levels were significantly reduced and fatigue was slowed down, whereas the limb grip strength and weight of mice were markedly increased compared with the saline-treated mdx mice. Furthermore, significantly reduced inflammation and necrosis areas were observed in the muscle tissues of mice in the AAV9-VEGF group. These results suggested that AAV9-mediated VEGF gene overexpression was able to improve the muscle damage in mdx mice.
杜兴氏肌营养不良症（DMD）是一种由肌营养不良蛋白缺失引起的致命性神经肌肉疾病。血管内皮生长因子（VEGF）是一种肝素结合二聚体糖蛋白，是刺激内皮细胞迁移、增殖和各种基因表达的主要血管生成因子。最近，VEGF被证明具有抗凋亡和直接的生肌作用，以及增强创伤性损伤后肌肉力量的恢复。因此，本研究试图评估mdx小鼠中VEGF过表达对肌肉损伤的影响。将腺相关病毒9型（AAV9）-VEGF静脉注射给mdx小鼠。注射后4周，观察到胫前肌中VEGF上调。此外，血清肌酸激酶水平显著降低，疲劳减缓，与生理盐水处理的mdx小鼠相比，小鼠的肢体握力和体重显著增加。此外，在AAV9-VEGF组小鼠的肌肉组织中观察到炎症和坏死区域明显减少。这些结果表明，AAV9介导的VEGF基因过表达能够改善mdx小鼠的肌肉损伤。
