仙茅苯甲酸酯类酚苷对维甲酸致大鼠骨质疏松症的影响

Effects of Benzylbenzoate Glucosides from Curculigo orchioides Gaertn. on Retinoic Acid Induced Osteoporosis in Rats

目的探讨仙茅苯甲酸酯类酚苷对维甲酸致大鼠骨质疏松症的作用。方法 3月龄SD雌性大鼠灌胃给予70 mg·kg-1·d-1的维甲酸造模2周,造模结束后给予雌二醇(E2,1 mg·kg-1)、淫羊藿总黄酮(TF,100 mg·kg-1)、仙茅苯甲酸酯类总酚苷(COP,6,18和54 mg·kg-1)、仙茅乙醇提取物(COE,3 000 mg·kg-1)4周。利用双能X线骨密度仪测右侧股骨的骨密度;全自动生化分析仪测定血清和尿液中Ca、P、肌酐(creatinine,Cr)含量及碱性磷酸酶(ALP)和抗酒石酸酸性磷酸酶(TRAP)的活性。以Elisa试剂盒测定血清中骨钙素(BGP)和脱氧吡啶啉(DPD)的水平。结果 SD雌性大鼠灌胃给予70mg·kg-1·d-1的维甲酸2周可显著降低大鼠股骨的骨密度,增加尿液中Ca与肌酐的比值和血清抗酒石酸酸性磷酸酶的活性。雌二醇、淫羊藿总黄酮和仙茅苯甲酸酯类总酚苷不仅可显著增加维甲酸骨质疏松大鼠的骨密度,降低尿液中Ca与肌酐的比值和抗酒石酸酸性磷酸酶活性,抑制骨吸收;还可调节维甲酸模型大鼠血清中骨钙素的水平,增加碱性磷酸酶的活性,促进骨形成。结论仙茅苯甲酸酯类酚苷可通过抑制骨吸收、增加骨形成减少维甲酸骨质疏松大鼠的骨丢失。

OBJECTIVE To investigate the therapeutic effects of benzylbenzoate glucosides from Curculigo orchioides on retinoic acid induced osteoporosis in rats. METHODS 3-Month-old female Sprague-Dawley rats were intragastrically given the retinoic acid 70 mg ~ kg-j ~ d-1 for 2 weeks, and then treated with estrogen（E2, 1 mg ~ kg-1 ）, total flavonoids from Epimediumfolium（TF, 100 mg ~ kg-l）, benzylbenzoate glucosides from Curculigo orchioides （COP,6,18 and 54 mg ~ kg-l） and Curculigo orchioides extracts （ COE,3 000 mg ~ kg-1 ）for 4 weeks, respectively. The bone mineral density of right femur were assayed by Dual Energy X-ray Ab- sorptiometry. The levels of Ca, P, creatinine, ALP and TRAP in serum and urine were assayed with automatic biochemical analyzer. The levels of BGP and DPD in serum were measured with Elisa kit according to instruction. RESULTS Treatment SD rats with retin- oic acid for 2 weeks significantly decreased bone mineral density, increased the ratio of Ca and Creatinine in urine, and serum TRAP activity. Treatment with E2 , TF and COP not only increased the bone mineral density, decreased the ratio of Ca and creatinine in urine and serum TRAP activity, but also regulated BGP level and increased ALP activity of serum in retinoic acid induced osteoporotic rats. CONCLUSION Benzylbenzoate glucosides from Curculigo orchioides can decrease bone loss by inhibiting bone resorption and impro- ving bone formation.