Pulsed electromagnetic fields (PEMF) attenuate changes in vertebral bone mass, architecture and strength in ovariectomized mice
Pulsed electromagnetic fields (PEMF) attenuate changes in vertebral bone mass, architecture and strength in ovariectomized mice
复制标题
脉冲电磁场 (PEMF) 减弱卵巢切除小鼠椎骨骨量、结构和强度的变化
DOI：
10.1016/j.bone.2017.12.008
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发表时间：
2018-03-01
期刊：
影响因子：
4.1
通讯作者：
Shen, Guanghao
中科院分区：
文献类型：
--
作者：
Lei, Tao;Liang, Zhuowen;Shen, Guanghao
脉冲电磁场（PEMF）已被研究作为预防绝经后骨质疏松症（OP）骨质流失的非侵入性替代方法，这些研究涉及的骨组织通常是OP患者或大鼠模型中的股骨和胫骨等长骨。然而，很少有研究调查 PEMF 对 OP 小鼠椎骨的影响。本研究旨在探讨PEMF是否能保留卵巢切除（OVX）小鼠OP模型中的腰椎骨量、微结构和强度及其相关机制。将 30 只 3 月龄雌性 BALB/c 小鼠随机分为三组 (n = 10)：假手术对照组 (Sham)、卵巢切除术 (OVX) 和卵巢切除联合 PEMF 治疗组 (OVX + PEMF)。 OVX + PEMF 组暴露于 15 Hz、1.6 mT PEMF，每周 7 天，每天 8 小时。 8周后，处死小鼠。与OVX组相比，OVX+PEMF组显示雌激素缺乏引起的小鼠体重增加较低。血清生化分析显示，OVX+PEMF组血清骨形成标志物骨特异性碱性磷酸酶（BALP）、血清骨钙素（OCN）、骨保护素（OPG）和I型前胶原N端前肽（P1NP）明显高于OVX组。此外，OVX+PEMF组血清骨吸收标志物抗酒石酸酸性磷酸酶5b（TRAP-5b）和I型胶原C端交联端肽（CTX-I）显着低于OVX组。生物力学测试观察到OVX+PEMF组与OVX组相比表现出更高的腰椎压缩最大载荷和刚度。腰椎微计算机断层扫描 (pCT) 和组织学分析表明，PEMF 部分阻止了 OVX 诱导的腰椎骨小梁骨量减少和骨小梁微结构恶化。实时PCR显示，与OVX组相比，OVX+PEMF组腰椎经典Wnt信号通路Wnt3a、LRP5和13catenin显着上调。此外,与OVX组相比,OVX+PEMF组RANKL和OPG mRNA表达量显着上调,而OVX+PEMF组与OVX组之间RANKL/OPG mRNA比值无统计学差异。此外，我们的研究还发现，与OVX组相比，OVX+PEMF组的RANK mRNA表达下调。综上所述，我们报告说，PEMF 治疗的长期刺激能够通过增加骨形成和抑制与调节 Wnt3a/LRP5/13catenin 和 OPG/RANKL/RANK 信号通路的骨骼基因表达相关的骨吸收来减轻绝经后小鼠的腰椎 OP。 (C) 2017 年，爱思唯尔公司出版
Pulsed electromagnetic fields (PEMF) has been investigated as a noninvasive alternative method to prevent bone loss for postmenopausal osteoporosis (OP), and the bone tissue involved in these studies are usually long bones such as femur and tibia in OP patients or rat models. However, few studies have investigated the effects of PEMF on the vertebral bone in mice with OP. This study aimed to investigate whether PEMF preserve lumbar vertebral bone mass, microarchitecture and strength in ovariectomized (OVX) mouse model of OP and its associated mechanisms. Thirty 3-month-old female BALB/c mice were randomly divided into three groups (n = 10): sham operated control (Sham), ovariectomy (OVX), and ovariectomy with PEMF treatment (OVX + PEMF). The OVX + PEMF group was exposed to 15 Hz, 1.6 mT PEMF for 8 h/day, 7 days/week. After 8 weeks, the mice were sacrificed. The OVX + PEMF group showed lower body weight gain of mice induced by estrogen deficiency compared with OVX group. Biochemical analysis of serum demonstrated that serum bone formation markers including bone specific alkaline phosphatase (BALP), serum osteocalcin (OCN), osteoprotegerin (OPG) and N-terminal propeptide of type I procollagen (P1NP) were markedly higher in OVX + PEMF group compared with OVX group. Besides, serum bone resorption markers including tartrate-resistant acid phosphatase 5b (TRAP-5b) and C terminal crosslinked telopeptides of type I collagen (CTX-I) were markedly lower in OVX + PEMF group compared with OVX group. Biomechanical test observed that OVX + PEMF group showed higher compressive maximum load and stiffness of the lumbar vertebrae compared with OVX group. Micro-computed tomography (pCT) and histological analysis of lumbar vertebrae revealed that PEMF partially prevented OVX-induced decrease of trabecular bone mass and deterioration of trabecular bone microarchitecture in lumbar vertebrae. Real-time PCR showed that the canonical Wnt signaling pathway of the lumbar vertebrae, including Wnt3a, LRP5 and 13catenin were markedly up-regulated in OVX + PEMF group compared with OVX group. Moreover, the mRNA expressions of RANKL and OPG were markedly up-regulated in OVX + PEMF group compared with OVX group, whereas no statistical difference in RANKL/OPG mRNA ratio was found between OVX + PEMF group and OVX group. Besides, our study also found that the RANK mRNA expression was down-regulated in OVX + PEMF group compared with OVX group. Taken together, we reported that long-term stimulation with PEMF treatment was able to alleviate lumbar vertebral OP in postmenopausal mice through a combination of increased bone formation and suppressed bone resorption related to regulating the skeletal gene expressions of Wnt3a/LRP5/13catenin and OPG/RANKL/RANK signaling pathways. (C) 2017 Published by Elsevier Inc.