Department of Orthopedics, Qilu Hospital of Shandong University and Spine and Spinal Cord Disease Research Center, Shandong University, Jinan, Shandong, China.
Department of Emergency Trauma Surgery, Linyi Central Hospital, Linyi, Shandong Province, China.
Biol Trace Elem Res. 2019 Aug;190(2):327-335. doi: 10.1007/s12011-018-1574-9. Epub 2018 Nov 12.
Silicon is one of the essential trace elements in the human body; the deficiency of which may lead to bone diseases. Numerous animal experiments have shown that an appropriate increase in the intake of silicon is beneficial to enhancing bone density and toughness to prevent osteoporosis. However, the molecular mechanisms of the silicon-mediated osteogenesis process have not been sufficiently clarified. In this study, we determined the possible osteogenesis-related mechanisms of orthosilicic acid at a molecular level. We detected the relevant pathway and osteogenic indicators by immunofluorescence (IF), Western blot, alkaline phosphatase (ALP) staining (using 5-bromo-4-chloro-3-indolyl phosphate/nitro blue tetrazolium [BCIP/NBT]), ALP enzyme labeling method, osteocalcin (OCN), and N-terminal propeptide of type 1 procollagen (P1NP) enzyme-linked immunosorbent assay (ELISA). We found that orthosilicic acid is capable of enhancing the expression of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), phospho-protein kinase B (P-Akt), phospho-mammalian target of rapamycin (P-mTOR), and related osteogenic markers (runt-related transcription factor 2 [RUNX2], type I collagen [COL1], ALP, OCN, and P1NP). However, with the addition of PI3K-Akt-mTOR pathway-specific inhibitor LY294002, the expression of PI3K, P-Akt, P-mTOR, RUNX2, COL1, ALP, OCN, and P1NP decreased. The results indicated that the PI3K-Akt-mTOR pathway played a positive regulatory role in the process of orthosilicic acid-mediated osteogenesis in vitro.
硅是人体必需的微量元素之一，其缺乏可能导致骨骼疾病。大量动物实验表明，适当增加硅的摄入量有利于提高骨密度和韧性，预防骨质疏松症。然而，硅介导的成骨过程的分子机制尚未得到充分阐明。在这项研究中，我们从分子水平上确定了正硅酸可能的成骨相关机制。我们通过免疫荧光（IF）、Western blot、碱性磷酸酶（ALP）染色（使用 5-溴-4-氯-3-吲哚磷酸/硝基蓝四唑[BCIP/NBT]）、ALP 酶标记法、骨钙素（OCN）和 1 型前胶原 N 端前肽（P1NP）酶联免疫吸附试验（ELISA）检测相关通路和成骨指标。我们发现正硅酸能够增强磷脂酰肌醇-4,5-二磷酸 3-激酶（PI3K）、磷酸蛋白激酶 B（P-Akt）、磷酸雷帕霉素靶蛋白（P-mTOR）及其相关成骨标志物（ runt 相关转录因子 2 [RUNX2]、I 型胶原[COL1]、ALP、OCN 和 P1NP）的表达。然而，加入 PI3K-Akt-mTOR 通路特异性抑制剂 LY294002 后，PI3K、P-Akt、P-mTOR、RUNX2、COL1、ALP、OCN 和 P1NP 的表达降低。结果表明，PI3K-Akt-mTOR 通路在正硅酸介导的体外成骨过程中发挥正向调节作用。
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