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Curr Mol Med. 2018 Mar 9;17(7):488-496. doi: 10.2174/1566524018666171219101142.

Puerarin Stimulates Osteogenic Differentiation and Bone Formation Through the ERK1/2 and p38-MAPK Signaling Pathways.

Author information

1
Center of Craniofacial Orthodontics, Department of Oral and Cranio-Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, Shanghai 200011, China.
2
Department of Pediatric Dentistry, Shanghai 9th People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology; National Clinical Research Center of Stomatology, Shanghai 200011, China.
3
2nd Dental Center, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, Shanghai 200011, China.

Abstract

BACKGROUND:

Osteoporosis is a world-wide health problem, which leads to decreased bone strength and increased susceptibility to fractures. Puerarin, a phytoestrogen extracted from Pueraria lobata (Willd.) Ohwi, has been identified as a promising intervention for preventing bone loss and promoting bone regeneration. However, the underlying mechanisms for its anabolic action are still not clear. In the present study, we aimed to investigate the effect of puerarin on the osteogenic differentiation of bone marrow stromal cells (BMSCs) and the possible molecular mechanism mediating its action.

METHODS:

Bone marrow stromal cells (BMSCs) and intragastric administration on ovariectomized(OVX) rats were used to study the anti-osteoporotic function of puerarin. The involvement of mitogen-activated protein kinase (MAPK) signaling pathways was determined.

RESULTS:

Our results demonstrated that at optimal concentration, puerarin could promote osteogenic differentiation of BMSCs in vitro. This induction was mediated by MAPK signaling pathway. Further detailed study revealed that ERK1/2-Runx2 signaling pathway had more prominent effect than p38 signaling pathway in puerarin-induced differentiation of BMSCs toward the osteogenic phenotype. We also found that puerarin protected against reduction in bone mineral density and improved femur trabecular bone structure in ovariectomized rats.

CONCLUSION:

Our findings revealed the functional mechanism of puerarin in promoting osteogenic differentiation which involved ERK1/2 and p38-MAPK pathway and provided experimental evidence for the potential application of puerarin for estrogen replacement therapy of osteoporosis.

KEYWORDS:

MAPKs; Puerarin; bone marrow stromal cell; estrogen replacement therapy.; osteogenesis; osteoporosis

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