Fragility fractures are related to the loss of bone integrity and deteriorated morphology of osteocytes. Our previous studies have reported that low‐magnitude high‐frequency vibration (LMHFV) promoted osteoporotic fracture healing. As osteocytes are known for mechanosensing and initiating bone repair, we hypothesized that LMHFV could enhance osteoporotic fracture healing through enhancing morphological changes in the osteocyte lacuna‐canalicular network (LCN) and mineralization. A metaphyseal fracture model was established in female Sprague‐Dawley rats to investigate changes in osteocytes and healing outcomes from early to late phase post‐fracture. Our results showed that the LCN exhibited an exuberant outgrowth of canaliculi in the osteoporotic fractured bone at day 14 after LMHFV. LMHFV upregulated the E11, dentin matrix protein 1 (DMP1), and fibroblast growth factor 23 (FGF23), but downregulated sclerostin (Sost) in osteocytes. Moreover, LMHFV promoted mineralization with significant enhancements of Ca/P ratio, mineral apposition rate (MAR), mineralizing surface (MS/BS), and bone mineral density (BMD) in the osteoporotic group. Consistently, better healing was confirmed by microarchitecture and mechanical properties, whereas the enhancement in osteoporotic group was comparable or even greater than the normal group. This is the first report to reveal the enhancement effect of LMHFV on the osteocytes’ morphology and functions in osteoporotic fracture healing.
This study aimed to investigate the inhibitory effects of the different concentrations of Tanshinone IIA (Tan IIA) on the proliferation of human alveolar epithelial cell line A549 and its regulatory mechanism in epithelial-mesenchymal transition (EMT). The proliferation activity of cells was examined using the thiazolyl blue tetrazolium bromide (MTT) method. The changes in the expression of epithelial cell marker protein E-cadherin (E-cad) and interstitial marker protein alpha-smooth muscle actin (α-SMA) were detected using the cellular immunochemical method. The changes in cell morphology and ultrastructure were observed under the inverted microscope and transmission electron microscope, respectively. Western blot analysis was used to detect the expression of E-cad, α-SMA, Smad7, and Smad3. The MTT assay showed that the cell viability in the transforming growth factor beta 1 (TGF-β1) induced group was higher than that in the normal group, but the difference was not obvious. However, the cell viability of the Tan IIA-treated groups obviously decreased compared with the TGF-β1-induced and normal groups. Meanwhile, the expression of E-cad and Smad7 decreased, and the expression of α-SMA and Smad3 increased after A549 cells were induced by 5 ng/mL TGF-β1 for 24 h. However, their expression levels were close to the expression level of the control group after the cells were treated with Tan IIA for 24 h. In conclusion, the results demonstrated that Tan IIA could inhibit EMT of alveolar epithelial cells induced by TGF-β1, probably by regulating the expression of TGF-β/Smad pathway protein. Therefore, Tan IIA might serve as a potential anti-fibrosis drug in treating pulmonary fibrosis.
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