Chongqing Key Laboratory of Oral Diseases and Biomedical

Chongqing, China

Chongqing Key Laboratory of Oral Diseases and Biomedical

Chongqing, China
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You T.,Chongqing Medical University | You T.,Chongqing Key Laboratory of Oral Diseases and Biomedical | Wang L.,Chongqing Medical University | Wang L.,Chongqing Key Laboratory of Oral Diseases and Biomedical | And 4 more authors.
Chinese Journal of Tissue Engineering Research | Year: 2013

Background: Naringin can increase bonemorphogeneticprotein 2 gene expression and promote the proliferation and differentiation of multipotential stem cell line. In vitro cell experiment indicates that naringin can suppress osteoclast formation and anti-osteoporosis activity. Objective: To prepare a mouse calvarial bone culture model containing naringin and to observe the effect of naringin with different concentrations on the formation and function of osteoclasts. Methods: Calvarial bone was dissected out aseptically from the 4-day-old Sprague Dawley mice, and cultured in the culture medium containing 0, 1, 10 and 100 mg/L naringin. The effects of naringin on the number of tartrate-resistant acid phosphatase-positive osteoclast marker enzyme in calvarial bone and the concentration of calcium in the culture medium were detected after cultured for 1, 3, 7 and 10 days. Results and Conclusion: After cultured for 1 day, the number of tartrate-resistant acid phosphatase-positive cells in calvarial bones and the calcium concentration in the culture medium had no difference between the groups. After cultured for 3 and 7 days, the number of tartrate-resistant acid phosphatase-positive cells was decreased and the calcium concentration was increased with the increasing concentration of naringin. At 10 days after culturing, this trend was most obvious. It showed that naringin could affect the number and function of tartrate-resistant acid phosphatase-positive cells in calvarial bones, and this effect showed a significant time- and dose-depend manner. The results show that naringin can not only promote the proliferation of osteroclasts, but also reduce the differentiation of osteoclasts or accelerate the apoptosis.

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