Abstract
Objective(s): The aim of this study was to evaluate the effects of fisetin to promote osteogenic differentiation in mice bone marrow mesenchymal stem cells (BMSCs).Materials and Methods: In this study cytotoxicity and viability of fisetin was measured by MTT assay. The differentiation effects of fisetin on BMSCs into osteoblast was assessed with alkaline phosphatase (ALP) activity measurement. Alizarin red staining and Real time PCR for osteoblast specific marker, Osteocalcin (OCN) ,Osteopontin (OPN), Runt-related transcription factor 2 (RUNX2), ERK and MAPK were investigatedResults: The results showed that fisetin does not have toxicity effect on BMSCs and it causes cell proliferation; hence 200, 400 and 800 µg/ml of fisetin was selected for the assessment of differentiation progress. Alizarin red staining (ARS) showed that fisetin promotes osteogenic differentiation on BMSCs at 21st day; dependently also higher alkaline phosphates activity was observed in the treatment groups of 10 days culture, compared to the control groups. The evaluation of Real time -PCR result evaluated showed that OCN OPN, RUNX2,ERK and MAPK genes expressions were increased.Conclusion: The results of this method, showed that differentiation in bone marrow stem cells took place through p38 MAPK, and ERK1 gene activation.
Highlights
Osteoporosis is a kind of skeletal disease, it is characterized by a high risk of bone fragility and fracture, low bone mineral density and bone pain
The results showed that fisetin does not have toxicity effect on bone marrow mesenchymal stem cells (BMSCs) and it causes cell proliferation; 200, 400 and 800 μg/ml of fisetin was selected for the assessment of differentiation progress
Alizarin red staining (ARS) showed that fisetin promotes osteogenic differentiation on BMSCs at 21st day; dependently higher alkaline phosphates activity was observed in the treatment groups of 10 days culture, compared to the control groups
Summary
Osteoporosis is a kind of skeletal disease, it is characterized by a high risk of bone fragility and fracture, low bone mineral density and bone pain. Hormone replacement therapy (HRT) is the way for the treatment of osteoporosis and Estrogen, known as a tissue regulator such as bone (Nongmaithem et al, 2016) and plays a fundamental role in skeletal growth and bone homeostasis in both men and women (Niada et al, 2016). It controls the activity of bone-forming osteoblasts and bone-resorbing osteoclasts, the physiological effects of estrogen are mediated by estrogen receptors (Wang et al, 2016).
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