Department of Orthopedics, The First Affiliated Hospital of Wannan Medical College, Yijishan Hospital, No. 2, Zhe Shan Xi Road, Wuhu, 241001, Anhui, PR China.
Anhui Province Key Laboratory of Non-coding RNA Basic and Clinical Transformation, No. 2, Zhe Shan Xi Road, Wuhu, 241001, Anhui, PR China.
J Mater Sci Mater Med. 2024 Oct 15;35(1):64. doi: 10.1007/s10856-024-06803-0.
More recently, increased studies have revealed that antioxidants can cure osteoporosis by inhibiting oxidative stress. Tauroursodeoxycholic acid (TUDCA) and Selenium (Se) have been confirmed to possess potent anti-oxidative effects and accelerate bone regeneration. In addition, very little is currently known about the effects of a combination with Se and TUDCA on bone defects in osteoporotic states. We, therefore, aimed to assess the protective effect of combination with Se and TUDCA on bone regeneration and investigate the effect and underlying mechanisms. When MC3T3-E1 was cultured in the presence of HH, Se, TUDCA and Se/TUDCA therapy could increase the matrix mineralization and promote expression of anti-oxidative stress markers in MC3T3-E1, while reducing intracellular reactive oxygen species (ROS) and mitochondrial ROS levels. Meanwhile, silent information regulator type 1 (SIRT1) was upregulated in response to Se, TUDCA and Se/TUDCA exposures in HH treated-MC3T3-E1. In the OVX rat model, Se, TUDCA and Se/TUDCA showed a clear positive effect against impaired bone repair in osteoporosis. The results above demonstrate that Se/TUDCA exhibits superior efficacy in both cellular and animal experiments, as compared to Se and TUDCA. In conclusion, combination with Se and TUDCA stimulates bone regeneration and is a promising candidate for promoting bone repair in osteoporosis.
最近，越来越多的研究表明抗氧化剂可以通过抑制氧化应激来治疗骨质疏松症。牛磺熊脱氧胆酸（TUDCA）和硒（Se）已被证实具有强大的抗氧化作用，并能加速骨再生。此外，目前对于 Se 和 TUDCA 联合应用于骨质疏松状态下骨缺损的效果知之甚少。因此，我们旨在评估 Se 和 TUDCA 联合应用对骨再生的保护作用，并研究其作用机制。当 MC3T3-E1 在 HH 存在的情况下培养时，Se、TUDCA 和 Se/TUDCA 治疗可以增加基质矿化并促进 MC3T3-E1 中抗氧化应激标志物的表达，同时降低细胞内活性氧（ROS）和线粒体 ROS 水平。同时，沉默信息调节因子 1（SIRT1）在 HH 处理的 MC3T3-E1 中对 Se、TUDCA 和 Se/TUDCA 的暴露作出反应而上调。在去卵巢大鼠模型中，Se、TUDCA 和 Se/TUDCA 对骨质疏松症中受损的骨修复表现出明显的积极作用。上述结果表明，与 Se 和 TUDCA 相比，Se/TUDCA 在细胞和动物实验中均具有更好的疗效。总之，Se 和 TUDCA 的联合应用刺激骨再生，是促进骨质疏松症骨修复的有前途的候选药物。
