Guangzhou University of Chinese Medicine, Guangzhou 510405, China; Lingnan Medical Research Center of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Guangzhou Medical University, Guangzhou, Guangdong 510260, China; Department of Spine Surgery, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510260, China.
Biomed Pharmacother. 2024 Jun;175:116571. doi: 10.1016/j.biopha.2024.116571. Epub 2024 Apr 26.
Diabetes can lead to a disorder of bone-fat balance, a significant cause of osteoporosis due to changes in environmental factors. Baicalin (Bai), an active ingredient of Scutellaria baicalensis, has been confirmed to possess antioxidant, hypoglycemic, and anti-osteoporotic effects. However, a comprehensive understanding of Bai's influence on diabetic osteoporosis (DOP), including its effects and underlying mechanisms, remains elusive. This study investigated Bai's impact on the bone-fat equilibrium in rats with DOP. The results indicated that Bai alleviated bone damage in DOP by promoting osteogenesis and inhibiting adipogenesis. Concurrently, through bioinformatics analysis, it was suggested that Bai's mechanism of action might involve the P38-MAPK pathway. In vitro, Bai was found to enhance the development of bone marrow mesenchymal stem cells (BMSCs) towards osteogenic lineages while suppressing their differentiation towards adipogenic lineages. It was discovered that Bai's promotion of BMSC osteogenic differentiation depends on the P38-MAPK pathway. Additionally, the synergistic effect mediated by Bai and P38-MAPK inhibitor suppressed BMSC adipogenic differentiation. Our research indicates that the P38-MAPK pathway play a role in Bai's effects on the osteogenic-adipogenic differentiation of BMSCs, showcasing the potential for DOP treatment. This study highlights Bai's ability to regulate the equilibrium between bone and fat, presenting a novel approach to adressing DOP.
糖尿病可导致骨-脂平衡紊乱，环境因素改变是骨质疏松症的重要原因。黄芩苷（Bai）是黄芩的一种活性成分，已被证实具有抗氧化、降血糖和抗骨质疏松作用。然而，对于 Bai 对糖尿病性骨质疏松症（DOP）的影响，包括其作用和潜在机制，仍缺乏全面的了解。本研究探讨了 Bai 对 DOP 大鼠骨-脂平衡的影响。结果表明，Bai 通过促进成骨和抑制成脂来减轻 DOP 中的骨损伤。同时，通过生物信息学分析，提示 Bai 的作用机制可能涉及 P38-MAPK 通路。在体外，Bai 被发现可增强骨髓间充质干细胞（BMSCs）向成骨谱系的发育，同时抑制其向成脂谱系的分化。发现 Bai 促进 BMSC 成骨分化依赖于 P38-MAPK 通路。此外，Bai 和 P38-MAPK 抑制剂介导的协同作用抑制了 BMSC 成脂分化。我们的研究表明，P38-MAPK 通路在 Bai 对 BMSCs 成骨-成脂分化的影响中起作用，为 DOP 的治疗提供了新的思路。本研究强调了 Bai 调节骨-脂平衡的能力，为治疗 DOP 提供了一种新方法。
