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J Nat Med ; 73(1): 104-113, 2019 Jan.
Article in English | MEDLINE | ID: mdl-30218208

ABSTRACT

Osteoporosis is characterized by low bone mass and the degeneration of bone structure, conditions which increase the risk of fracture. Aloin has been shown to affect bone metabolism, but its role in osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) remains unclear. The aim of our study was to determine whether aloin promotes the proliferation and osteogenic differentiation of BMSCs and, if so, whether it acts via activation of the ERK1/2-Runx2 signaling pathway. We found that the different concentrations of aloin tested had no obvious cytotoxic effects on the viability of BMSCs. Under osteogenic induction conditions, aloin increased cellular alkaline phosphatase activity, promoted BMSC mineralization, and increased osteogenic-related gene expression. In addition, treating the BMSCs with the signal transduction inhibitor PD98059 (ERK1/2) effectively attenuated Runx2 activation in these cells and also suppressed osteoblastic differentiation. Overall, our study demonstrates that aloin promotes osteogenic differentiation of BMSCs through activation of the ERK1/2-Runx2 signaling pathway.


Subject(s)
Core Binding Factor Alpha 1 Subunit/metabolism , Emodin/analogs & derivatives , Mesenchymal Stem Cells/cytology , Osteogenesis/drug effects , Signal Transduction , Animals , Bone Marrow , Cell Differentiation , Cells, Cultured , Emodin/pharmacology , Extracellular Signal-Regulated MAP Kinases/metabolism , Flavonoids/pharmacology , Mesenchymal Stem Cells/drug effects , Rats , Rats, Sprague-Dawley
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