Zhen-Xiong Jin1,2, Xin-Yuan Liao3, Wei-Wei Da1,2, Yong-Jian Zhao1,2, Xiao-Feng Li1,2, De-Zhi Tang4,5. 1. Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. 2. Institute of Spine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. 3. Spine Center, Department of Orthopaedics, Shanghai Changzheng Hospital, Navy Medical University, Shanghai, 201705, China. 4. Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. dztang702@126.com. 5. Institute of Spine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. dztang702@126.com.
Abstract
INTRODUCTION: Osthole has a potential therapeutic application for anti-osteoporosis. The present study verified whether osthole downregulates osteoclastogenesis via targeting OPG. METHODS: In vivo, 12-month-old male mice were utilized to evaluate the effect of osthole on bone mass. In vitro, bone marrow stem cells (BMSCs) were isolated and extracted from 3-month-old OPG-/- mice and the littermates of OPG+/+ mice. Calvaria osteoblasts were extracted from 3-day-old C57BL/6J mice or 3-day-old OPG-/- mice and the littermates of OPG+/+ mice. RESULTS: Osthole significantly increased the gene and protein levels of OPG in primary BMSCs in a dose-dependent manner. The deletion of the OPG gene did not affect β-catenin expression. The deletion of the β-catenin gene inhibited OPG expression in BMSCs, indicating that osthole stimulates the expression of OPG via activation of β-catenin signaling. CONCLUSION: Osthole attenuates osteoclast formation by stimulating the activation of β-catenin-OPG signaling and could be a potential drug for the senile osteoporosis.
INTRODUCTION:Osthole has a potential therapeutic application for anti-osteoporosis. The present study verified whether osthole downregulates osteoclastogenesis via targeting OPG. METHODS: In vivo, 12-month-old male mice were utilized to evaluate the effect of osthole on bone mass. In vitro, bone marrow stem cells (BMSCs) were isolated and extracted from 3-month-old OPG-/- mice and the littermates of OPG+/+ mice. Calvaria osteoblasts were extracted from 3-day-old C57BL/6J mice or 3-day-old OPG-/- mice and the littermates of OPG+/+ mice. RESULTS:Osthole significantly increased the gene and protein levels of OPG in primary BMSCs in a dose-dependent manner. The deletion of the OPG gene did not affect β-catenin expression. The deletion of the β-catenin gene inhibited OPG expression in BMSCs, indicating that osthole stimulates the expression of OPG via activation of β-catenin signaling. CONCLUSION:Osthole attenuates osteoclast formation by stimulating the activation of β-catenin-OPG signaling and could be a potential drug for the senile osteoporosis.
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