Department of Orthopaedic Trauma, The First Hospital of Jilin University, Changchun, Jilin, China.
Department of Radiology, The First Hospital of Jilin University, Changchun, Jilin, China.
J Orthop Surg Res. 2021 Oct 30;16(1):650. doi: 10.1186/s13018-021-02803-w.
Low-magnitude high-frequency vibration (LMHFV) has been reported to be capable of promoting osteoblast proliferation and differentiation. Reduced osteoblast activity and impaired bone formation were related to diabetic bone loss. We investigated the potential protective effects of LMHFV on high-glucose (HG)-induced osteoblasts in this study. In addition, the assessment of LMHFV treatment for bone loss attributed to diabetes was also performed in vivo.
MC3T3-E1 cells induced by HG only or treated with LMHFV were treated in vitro. The experiments performed in this study included the detection of cell proliferation, migration and differentiation, as well as protein expression. Diabetic bone loss induced by streptozotocin (STZ) in rats was established. Combined with bone morphometric, microstructure, biomechanical properties and matrix composition tests, the potential of LMHFV in treating diabetes bone loss was explored.
After the application of LMHFV, the inhibiting effects of HG on the proliferation, migration and differentiation of osteoblasts were alleviated. The GSK3β/β-catenin pathway was involved in the protective effect of LMHFV. Impaired microstructure and biomechanical properties attributed to diabetes were ameliorated by LMHFV treatment. The improvement of femur biomechanical properties might be associated with the alteration of the matrix composition by the LMHFV.
LMHFV exhibited a protective effect on osteoblasts against HG by regulating the proliferation, migration and differentiation of osteoblasts. The function of promoting bone formation and reinforcing bone strength made it possible for LMHFV to alleviate diabetic bone loss.
低频高幅振动(LMHFV)已被报道能够促进成骨细胞的增殖和分化。成骨细胞活性降低和骨形成受损与糖尿病性骨丢失有关。本研究旨在探讨 LMHFV 对高糖(HG)诱导的成骨细胞的潜在保护作用。此外,还在体内评估了 LMHFV 治疗糖尿病相关骨丢失的效果。
体外培养仅受 HG 诱导或经 LMHFV 处理的 MC3T3-E1 细胞。本研究进行的实验包括细胞增殖、迁移和分化检测以及蛋白表达分析。采用链脲佐菌素(STZ)诱导大鼠糖尿病性骨丢失模型。结合骨形态计量学、微结构、生物力学性能和基质组成测试,探索 LMHFV 治疗糖尿病性骨丢失的潜力。
应用 LMHFV 后,HG 对成骨细胞增殖、迁移和分化的抑制作用得到缓解。LMHFV 的保护作用涉及 GSK3β/β-catenin 通路。糖尿病引起的微结构和生物力学性能受损得到了 LMHFV 治疗的改善。股骨生物力学性能的提高可能与 LMHFV 改变基质组成有关。
LMHFV 通过调节成骨细胞的增殖、迁移和分化,对成骨细胞具有保护作用,能促进骨形成和增强骨强度,从而有可能缓解糖尿病性骨丢失。