Effect of low-voltage electrical stimulation on angiogenic growth factors in ischaemic rat skeletal muscle
Effect of low-voltage electrical stimulation on angiogenic growth factors in ischaemic rat skeletal muscle
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DOI：
10.1111/j.1440-1681.2006.04417.x
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发表时间：
2006-07-01
影响因子：
2.9
通讯作者：
Sato, Yasufumi
中科院分区：
文献类型：
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作者：
Nagasaka, Makoto;Kohzuki, Masahiro;Sato, Yasufumi
1.低电压电刺激（LVES）在骨骼肌中的水平远低于肌肉收缩的阈值已被报道，以促进局部血管生成。然而，LVES促进局部血管生成的机制尚未完全阐明。在本研究中，我们评估了血管生成因子，如血管内皮生长因子（VEGF），肝细胞生长因子（HGF）和成纤维细胞生长因子（FGF），以及其他不利因素，如炎症（白细胞介素（IL）-6）和缺氧（缺氧诱导因子（HIF）-1 α），是否有助于局部血管生成。我们完全切除雄性Sprague-Dawley大鼠的双侧股动脉。手术后，将电极植入双侧胫骨前肌（TA）筋膜中心，皮下隧道，并在肩胛骨水平外置。以50 Hz的刺激频率、0.1 V的刺激强度和无间隔连续刺激大鼠右侧TA肌肉5 d。左侧TA肌作为对照。我们发现，VEGF和HGF蛋白在刺激的肌肉与对照组相比，LVES显着增加。ELISA法检测LVES组VEGF水平为89.10 ± 17.19 ng/g，对照组为65.07 ± 12.88 ng/g（P < 0.05）。LVES组和对照组的HGF水平分别为8.52 ± 1.96和5.80 ± 2.14 ng/g（P < 0.05）。相比之下，LVES组和对照组之间的FGF、IL-6和HIF-1 α无差异.这些结果表明，LVES在大鼠后肢缺血模型中不仅增加VEGF，而且增加HGF的产生，这可能是负责由LVES产生的血管生成的主要机制。
1. Low-voltage electrical stimulation (LVES) in skeletal muscle at a level far below the threshold of muscle contraction has been reported to promote local angiogenesis. However, the mechanism underlying the promotion of local angiogenesis by LVES has not been fully elucidated. In the present study, we evaluated whether angiogenic factors, such as vascular endotherial growth factor (VEGF), hepatocyte growth factor (HGF) and fibroblast growth factor (FGF), as well as other disadvantageous factors, such as inflammation (interleukin (IL)-6) and hypoxia (hypoxia-inducible factor (HIF)-1 alpha), contribute to the local angiogenesis produced by LVES.2. We completely excised bilateral femoral arteries of male Sprague-Dawley rats. After the operation, electrodes were implanted onto the centre of the fascia of the bilateral tibialis anterior (TA) muscles, tunnelled subcutaneously and exteriorized at the level of the scapulae. The right TA muscles of rats were stimulated continuously at a stimulus frequency of 50 Hz, with a 0.1 V stimulus strength and no interval, for 5 days. The left TA muscles served as controls.3. We found that both VEGF and HGF protein were significantly increased by LVES in stimulated muscles compared with control. The VEGF level of the LVES group was 89.10 +/- 17.19 ng/g, whereas that of the control group was 65.07 +/- 12.88 ng/g, as determined by ELISA (P < 0.05). The HGF level of the LVES and control groups was 8.52 +/- 1.96 and 5.80 +/- 2.14 ng/g, respectively (P < 0.05). In contrast, there was no difference in FGF, IL-6 and HIF-1 alpha between the LVES and control groups.4. These results suggest that LVES in a hindlimb ischaemia model of rats increases not only VEGF, but also HGF, production, which may be the main mechanism responsible for the angiogenesis produced by LVES.