DSS调节内脂素防治去卵巢大鼠骨基质丢失的研究

DSS Sustains Bone Matrix of Ovariectomized Rats by Regulating Visfatin

目的:探讨3'-大豆苷元磺酸钠(3'-daidzein sulfonate sodium,DSS)调节内脂素防治去卵巢大鼠骨基质丢失的作用。方法:选择清洁级SD雌性大鼠60只,体重160~220 g,随机分成5组:1假手术组(正常对照组),2卵巢切除组(模型组),3卵巢切除+戊酸雌二醇组(阳性药物对照组),4卵巢切除+DSS高剂量组(100μg·kg^(^(-1))),5卵巢切除+DSS低剂量组(30μg·kg^(^(-1)))。术后1周连续阴道涂片检查10天后,12组大鼠每天灌胃同体积生理盐水;3组大鼠每天一次戊酸雌二醇片剂水溶悬液灌胃,剂量为80 mg·kg^(^(-1));45组分别以高、低剂量的DSS溶液灌胃,1次·d^(^(-1))。连续给药8周。大鼠禁食12 h,麻醉后腹主动脉取血并分离血清,严格按照试剂盒说明,用ELISA方法检测血清中内脂素(Visfatin)的含量,化学比色法测定血清中STr ACP含量。另取实验大鼠右股骨,以浓硝酸消化后火焰原子吸收光谱法检测骨钙、骨镁浓度。结果:与模型组比较,DSS可升高骨钙、骨镁浓度,降低血清内Visfatin及STr ACP含量,差异有统计学意义。结论:DSS可能通过调节内脂素预防大鼠去卵巢后因雌激素缺乏所致的骨基质丢失,其作用机制可能通过调节内脂素的联动效应达到维持大鼠骨代谢平衡。

Objective： To study the effect of 3 ＇-daidzein sulfonate sodium（ DSS） on sustaining the bone matrix of ovariectomized rats. Methods： Sixty SD female rats with weight between 160 ～ 220 g were randomly divided into 5 groups： 1sham group（ control group）; 2 ovariectomy group（ model group）; 3 ovariectomy ＋ estradiol valerate treatment group（ positive control group）; 4ovariectomy ＋ high-dose DSS（ 100 μg·kg（-1））; 5 ovariectomy ＋ low-dose DSS（ 30 μg·kg（-1））. Vaginal smear was examined consecutively for 10 days one week after surgery. 12 Group were gavaged with the same volume saline; 3group were gavaged with estradiol valerate solution（ 80 mg·kg（-1）） once per day; 45 group were gavaged with high-and low-dose DSS solution once per day. All the rats were gavaged for 8 weeks and starved for 12 hours before anesthesia. Abdominal aortic blood was taken from anesthetized rats and serum was isolated to measure visfalin level using ELISA kit. The serum STr ACP level was also assessed by chemical colorimetric method. The right femur was excised,and digested with concentrated nitric acid for bone calcium and magnesium measurement using the flame atom absorption method. Results： DSS treatment increased the level of bone calcium and magnesium,and reduced the concentration of visfatin and STr ACP. The comparison between the model group and DSS treatment groups was statistically significant. Conclusion： DSS can regulate visfatin to prevent the loss of bone matrix caused by estrogen insufficiency post ovariectomy. A possible mechanism for this effect might rely on the coupling effect of visfatin regulation to maintain the osseous homeostasis.