2. Academic Validation
  3. Mogroside V enhances bone marrow mesenchymal stem cells osteogenesis under hyperglycemic conditions through upregulating miR-10b-5p and PI3K/Akt signaling

Mogroside V enhances bone marrow mesenchymal stem cells osteogenesis under hyperglycemic conditions through upregulating miR-10b-5p and PI3K/Akt signaling

  • J Orthop Surg Res. 2025 Mar 14;20(1):278. doi: 10.1186/s13018-025-05684-5.
Dongni Lan # 1 2,  Kongmei Li # 1 2,  Zhimao Ye 1 2,  Yicai Luo 1 2,  Cuiping Li 1 2,  Hao Li 3 4
Affiliations

Affiliations

  • 1 Department of Prosthodontics, College & Affiliated Hospital of Stomatology, Guangxi Medical University, Nanning, 530021, Guangxi, China.
  • 2 Guangxi Key Laboratory of Oral and Maxillofacial Restoration and Reconstruction, Guangxi Medical University, Nanning, 530021, Guangxi, China.
  • 3 Department of Prosthodontics, College & Affiliated Hospital of Stomatology, Guangxi Medical University, Nanning, 530021, Guangxi, China. sherrylee2011@126.com.
  • 4 Guangxi Key Laboratory of Oral and Maxillofacial Restoration and Reconstruction, Guangxi Medical University, Nanning, 530021, Guangxi, China. sherrylee2011@126.com.
  • # Contributed equally.
PMID: 40082984 DOI: 10.1186/s13018-025-05684-5
Abstract

Background: Mogroside V (MV) is a triterpene glucoside that reportedly exhibits an array of antitumor, anti-inflammatory, hypolipidemic, and hypoglycemic properties. In prior studies, our group determined that MV was able to readily enhance osteogenic bone marrow mesenchymal stem cells (BMSCs) differentiation under high-glucose conditions through mechanisms potentially associated with miR-10b-5p and PI3K/Akt signaling activity. The precise molecular basis for these effects, however, remains to be fully elucidated.

Objective: This study aims to explore the potential mechanisms by which MV regulates the osteogenic differentiation of BMSCs under hyperglycemic conditions.

Methods: Femoral and tibial BMSCs were isolated from control and diabetic C57BL/6J mice. qRT-PCR was used to quantify miR-10b-5p levels. Putative miR-10b-5p target genes were predicted through bioinformatics assays and validated in a luciferase reporter assay system. miR-10b-5p expression was inhibited with an antagomiR-10b-5p construct, while PI3K/Akt pathway signaling was inhibited with LY294002. Western blotting was used to detect PI3K/Akt pathway and target gene protein levels, while Alizarin red staining was used to detect calcium nodule deposition by BMSCs.

Results: miR-10b-5p upregulation was noted in BMSCs exposed to hyperglycemic conditions. HOXD10 was identified as a cell differentiation-related miR-10b-5p target gene in bioinformatics analyses, and the targeting relationship between the two was confirmed in a luciferase reporter assay. MV treatment elicited significantly higher levels of miR-10b-5p expression, PI3K phosphorylation, and calcium deposition, while antagomiR-10b-5p or LY294002 treatment reversed these changes, and the opposite trends were observed with respect to HOXD10 protein levels.

Conclusion: MV favors BMSCs osteogenic differentiation under high-glucose conditions through the upregulation of miR-10b-5p and the activation of PI3K/Akt signaling.

Keywords

Bone marrow mesenchymal stem cells; Diabetes; Mogroside V; Osteogenic differentiation; PI3K/Akt; miR-10b-5p.

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