Naringin intervention influences the formation and function of osteoclasts from mouse calvarial bone
10.3969/j.issn.2095-4344.2013.37.004
- VernacularTitle:柚皮甙干预鼠颅顶骨破骨细胞的形成及功能
- Author:
Tao YOU
;
Lu WANG
;
Yan JI
;
Xiaohong WU
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2013;(37):6561-6566
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Naringin can increase bonemorphogeneticprotein 2 gene expression and promote the proliferation and differentiation of multipotential stem cel line. In vitro cel 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 aseptical y 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 cel s 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 cel s 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 cel s 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.