VK2 Promotes Osteogenic Differentiation of BMSCs against High Glucose Exposure via Modulation of Intracellular Oxidative Stress

Author:

Fang Wenlai123,Lv Yiyun34,Jin Shuqing34,Zhu Zheng34,Chen Yunzhen1ORCID

Affiliation:

1. Department of Orthopedics, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, China

2. Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325000, China

3. Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, 325000, China

4. The Second Clinical Medical College of Wenzhou Medical University, Wenzhou, 325000, China

Abstract

Introduction: Diabetic osteoporosis (DOP) has gradually gained public attention. The clinical manifestations of DOP include bone mass loss, bone microstructural damage, and increased bone fragility. Methods: Intracellular reactive oxygen species (ROS) production was significantly increased under high glucose (HG) conditions, with deleterious effects on bone mesenchymal stem cells (BMSCs) proliferation and osteogenic differentiation. Vitamin K2 (VK2) has been demonstrated to promote bone formation both in vitro and in vivo. Results: However, its potential role in diabetes-induced osteoporosis remains unelucidated. This study aims to verify whether VK2 treatment could relieve the deleterious effects of high glucose on BMSCs and delay the progression of osteoporosis. The results revealed that the HG environment downregulated the expression of osteogenesis- related proteins. Conclusion: Correspondingly, VK2 treatment reversed the osteogenic phenotype of BMSCs under HG conditions. In addition, using an established diabetes-induced osteoporosis rat model, we found that VK2 administration could restore bone mass and microstructure. In conclusion, our results provide a promising therapeutic option in the clinical treatment of DOP.

Publisher

Bentham Science Publishers Ltd.

Subject

Drug Discovery,Pharmacology

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