Qilu Hospital of Shandong University, Jinan, Shandong, China.
Department of Spine Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Biol Trace Elem Res. 2023 Feb;201(2):843-855. doi: 10.1007/s12011-022-03201-x. Epub 2022 Mar 21.
Glucocorticoid-induced osteoporosis (GIOP) has been the most common form of secondary osteoporosis. Glucocorticoids (GCs) can induce osteocyte and osteoblast apoptosis. Plenty of research has verified that silicon intake would positively affect bone. However, the effects of silicon on GIOP are not investigated. In this study, we assessed the impact of ortho-silicic acid (OSA) on Dex-induced apoptosis of osteocytes by cell apoptosis assays. The apoptosis-related genes, cleaved-caspase-3, Bcl-2, and Bax, were detected by western blotting. Then, we evaluated the possible role of OSA on osteogenesis and osteoclastogenesis with Dex using Alizarin red staining and tartrate-resistant acid phosphatase (TRAP) staining. We also detected the related genes by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and western blotting. We then established the GIOP mouse model to evaluate the potential role of OSA in vivo. We found that OSA showed no cytotoxic on osteocytes below 50 μM and prevented MLO-Y4 from Dex-induced apoptosis. We also found that OSA promoted osteogenesis and inhibited osteoclastogenesis with Dex. OSA had a protective effect on GIOP mice via the Akt signal pathway in vivo. In the end, we verified the Akt/Bad signal pathway in vitro, which showed the same results. Our finding demonstrated that OSA could protect osteocytes from apoptosis induced by GCs both in vitro and in vivo. Also, it promoted osteogenesis and inhibited osteoclastogenesis with the exitance of Dex. In conclusion, OSA has the potential value as a therapeutic agent for GIOP.
糖皮质激素诱导的骨质疏松症（GIOP）是最常见的继发性骨质疏松症。糖皮质激素（GCs）可诱导破骨细胞和成骨细胞凋亡。大量研究证实，硅的摄入对骨骼有积极影响。然而，硅对 GIOP 的影响尚未得到研究。在这项研究中，我们通过细胞凋亡实验评估了正硅酸（OSA）对 Dex 诱导的破骨细胞凋亡的影响。通过 Western blot 检测凋亡相关基因 cleaved-caspase-3、Bcl-2 和 Bax。然后，我们使用茜素红染色和抗酒石酸酸性磷酸酶（TRAP）染色用 Dex 评估 OSA 对成骨和破骨的可能作用。我们还通过定量逆转录聚合酶链反应（qRT-PCR）和 Western blot 检测相关基因。然后，我们建立了 GIOP 小鼠模型，以评估 OSA 在体内的潜在作用。我们发现 OSA 在低于 50μM 时对破骨细胞没有细胞毒性，并防止 MLO-Y4 受到 Dex 诱导的凋亡。我们还发现 OSA 促进了成骨并抑制了 Dex 诱导的破骨细胞形成。OSA 通过体内 Akt 信号通路对 GIOP 小鼠具有保护作用。最后，我们在体外验证了 Akt/Bad 信号通路，结果相同。我们的发现表明，OSA 可以在体外和体内保护破骨细胞免受 GCs 诱导的凋亡。此外，它在 Dex 的存在下促进成骨并抑制破骨细胞形成。总之，OSA 具有作为治疗 GIOP 的潜在价值。
