【摘要】 目的　探讨氟化钠对大鼠破骨样细胞及其凋亡的影响 ,进而推测地方性氟病的发病和氟化物治疗骨质疏松的机制。方法　以 5mg LNaF和 15mg LNaF饲喂正常和去卵巢 (OVX)大鼠 6个月 ,观察了体内和培养基中的NaF对大鼠破骨样细胞 (OLC)形成和凋亡的影响。结果　氟摄入 2个月时 ,15mg LNaF明显抑制正常和OVX大鼠OLC形成 ;第 5个月时 ,5mg LNaF和 15mg LNaF均抑制正常和OVX大鼠的OLC形成。氟摄入 2周时 ,发现NaF促进OVX大鼠OLC凋亡 ;1个月时 ,NaF促进正常和OVX大鼠OLC凋亡 ,随时间的延长 ,其促进作用逐渐增强。以上作用均表现为 15mg LNaF的作用明显大于 5mg LNaF。体外NaF抑制OLC形成并促进OLC凋亡 ,其作用程度为 15mg LNaF >10mg LNaF >5mg LNaF。结论　体内NaF抑制正常和OVX大鼠OLC的形成并促进正常和OVX大鼠OLC凋亡 ,其作用是时间和剂量依赖性的。培养基中NaF抑制OLC形成并促进正常和OVX大鼠OLC的凋亡 ,其作用是剂量依赖性的更多还原

【Abstract】 Objective It has been developed a method of osteoclast culture and observation of its’ apoptosis in vitro in order to unveil the mechanisms of endemic fluorosis asnd osteoporosis treatment by fluoride at cellular level. Methods Normal and OVX rats were fed on 5mg/L or 15mg/L NaF water. Investigations of osteoclast like cell(OLC)formation and its apoptosis in vitro in adult rat modulated by fluoride in vivo and the effects of 5,10,15 mg/L NaF on OLC formation and its apoptosis in vitro were carried out. Results Both 5 and 15mg/L NaF inhibited normal and OVX rat OLC formation in vitro 5 months after fluoride administration although the inhibition effect in 5 mg/L group was less than that in 15ml/L group.The inhibition effect in 15mg/L group was obvious even at 2 months.Fluoride promoted OVX rat OLC apoptosis at 2 weeks of NaF administration or later on.Both 5 and 15 mg/L NaF could promote normal and OVX rat OLC apoptosis from 2nd month after NaF administration.The promotion effects enhanced with increasing time, and were stronger in 15mg/L group than in of 5mg/L group.Conclusion Normal and OVX rat OLC formation in vitro were inhibited by NaF in vivo in dose time dependent manner.Normal and OVX rat OLC apoptosis in vitr o were promoted by NaF in vivo in dose time dependent manner.The OCL formation inhibition and apoptosis promotion effects of NaF in culture media on normal and OVX rat OLC apoptosis are dose dependent.The evidence presented in this paper may explain the reason that the observed reduction in osteoclast number is attributed to the reduction of osteoclast formation and induction of its apoptosis by sodium fluonite.更多还原