Effects of extracts of oxyntic mucosa in rat on the biological activity of osteoblasts

Summary We explored the relationship between extracts of oxyntic mucosa (EOM) and the biological activity of osteoblasts in rats. We found that EOM could enhance the activity of bone formation in osteoblast. Our results suggest that EOM likely play a role in the cases of osteopenia induced by gastre...

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Veröffentlicht in:Osteoporosis international 2010, Vol.21 (1), p.129-135
Hauptverfasser: Zhao, C.-Y, Chen, J.-T, Yang, D.-H, Zhong, Z.-M, Bai, L
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Sprache:eng
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Zusammenfassung:Summary We explored the relationship between extracts of oxyntic mucosa (EOM) and the biological activity of osteoblasts in rats. We found that EOM could enhance the activity of bone formation in osteoblast. Our results suggest that EOM likely play a role in the cases of osteopenia induced by gastrectomy. Introduction Surgical removal of the stomach (gastrectomy) leads to osteopenia in animals and in humans. It was demonstrated that EOM could induce transient hypocalcaemia and stimulate an uptake of Ca²⁺ into bone in rats. The main aim of this study has been to clarify whether this procedure was performed through osteoblast, which is responsible for bone formation. Methods Osteoblasts were isolated, cultured, and identified in vitro. Preparing the rats' EOM and diluting into low, middle, and high concentrations, respectively. After osteoblasts were treated by different concentration EOMs or saline (for control), the intracytoplasm [Ca²⁺]i was measured by laser scanning confocal microscopy; the proliferation of osteoblast cells were detected with cell counting kit 8 (CCK-8); and the expressions of collagen type I and osteocalcin were assayed by reverse transcriptase polymerase chain reaction and Western blot. Results EOMs were found to induce a dose-related rapid increase of intracytoplasm [Ca²⁺]i in osteoblasts and could stimulate osteoblasts to enhance proliferation and upregulate the expressions of collagen type I and osteocalcin significantly (p 
ISSN:0937-941X
1433-2965
DOI:10.1007/s00198-009-0928-8