Department of Orthopedics, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Department of Respiratory and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Mol Med Rep. 2020 Oct;22(4):3387-3395. doi: 10.3892/mmr.2020.11391. Epub 2020 Jul 30.
Metformin, a cost‑effective and safe orally administered antidiabetic drug used by millions of patients, has exhibited great interest for its potential osteogenic‑promoting properties in different types of cells, including mesenchymal stem cells (MSCs). Diabetic osteopathy is a common comorbidity of diabetes mellitus; however, the underlying molecular mechanisms of metformin on the physiological processes of MSCs, under high glucose condition, remain unknown. To determine the effects of metformin on the regulatory roles of proliferation and differentiation in MSCs, under high glucose conditions, osteogenesis after metformin treatment was detected with Alizarin Red S and ALP staining. The results demonstrated that high glucose levels significantly inhibited cell proliferation and osteogenic differentiation under high glucose conditions. Notably, addition of metformin reversed the inhibitory effects induced by high glucose levels on cell proliferation and osteogenesis. Furthermore, high glucose levels significantly decreased mitochondrial membrane potential (MMP), whereas treatment with metformin helped maintain MMP. Further analysis of mitochondrial function revealed that metformin significantly promoted ATP synthesis, mitochondrial DNA mass and mitochondrial transcriptional activity, which were inhibited by high glucose culture. Furthermore, metformin significantly scavenged reactive oxygen species (ROS) induced by high glucose levels, and regulated the ROS‑AKT‑mTOR axis inhibited by high glucose levels, suggesting the protective effects of metformin against high glucose levels via regulation of the ROS‑AKT‑mTOR axis. Taken together, the results of the present study demonstrated the protective role of metformin on the physiological processes of MSCs, under high glucose condition and highlighted the potential molecular mechanism underlying the effect of metformin in promoting cell proliferation and osteogenesis under high glucose condition.
二甲双胍是一种经济有效的口服抗糖尿病药物,为数百万患者所使用,因其在不同类型的细胞中具有潜在的成骨促进特性而备受关注,包括间充质干细胞 (MSCs)。糖尿病性骨病是糖尿病的常见合并症;然而,二甲双胍在高糖条件下对 MSCs 生理过程的潜在分子机制仍不清楚。为了确定二甲双胍对 MSCs 增殖和分化的调节作用,在高糖条件下用茜素红 S 和 ALP 染色检测了二甲双胍处理后的成骨作用。结果表明,高葡萄糖水平显著抑制了高糖条件下细胞的增殖和成骨分化。值得注意的是,添加二甲双胍逆转了高葡萄糖水平对细胞增殖和成骨的抑制作用。此外,高葡萄糖水平显著降低了线粒体膜电位 (MMP),而二甲双胍治疗有助于维持 MMP。进一步分析线粒体功能表明,二甲双胍显著促进了 ATP 合成、线粒体 DNA 质量和线粒体转录活性,而高糖培养抑制了这些活性。此外,二甲双胍显著清除了由高葡萄糖水平诱导的活性氧 (ROS),并调节了由高葡萄糖水平抑制的 ROS-AKT-mTOR 轴,表明二甲双胍通过调节 ROS-AKT-mTOR 轴对高葡萄糖水平具有保护作用。综上所述,本研究结果表明,二甲双胍在高糖条件下对 MSCs 的生理过程具有保护作用,并强调了二甲双胍在促进高糖条件下细胞增殖和成骨作用的潜在分子机制。