摘要
目的 探讨晚期糖化终末产物 (AGEs)在去卵巢大鼠骨质疏松发病中的作用及氨基胍防治效果。方法 选用 1 0月龄大鼠通过卵巢切除诱导骨质疏松并用氨基胍防治其骨量丢失 ,测定其骨密度及骨胶原中 AGEs的含量及血、尿生化指标。结果 卵巢切除大鼠骨密度 (0 .2 0 7g/cm2 ± 0 .0 1 6 g/cm2 )明显低于假手术大鼠 (0 .2 36 g/cm2 ± 0 .0 1 0 g/cm2 ) (P<0 .0 1 ) ,而骨胶原 AGEs含量 (59.86 RU/mg胶原± 3.1 3 RU/mg胶原 )明显高于假手术组大鼠 (53.83RU/mg胶原± 5.46RU/mg胶原 ) (P<0 .0 1 )。卵巢切除大鼠血清雌激素 (4.50 pg/ml± 1 .73pg/ml)与假手术组(8.45 pg/ml± 2 .90 pg/ml)比较明显降低 (P<0 .0 2 ) ,2 4 h尿钙、尿钙与肌酐比值、尿磷、尿磷与肌酐比值均有升高趋势。卵巢切除大鼠给予氨基胍后骨密度 (0 .2 2 1 g/cm2± 0 .0 1 7g/cm2 )明显升高 (P<0 .0 5) ,骨胶原中 AGEs含量 (51 .2 3RU/mg胶原± 7.46RU/mg胶原 )明显降低 (P<0 .0 1 ) ,血清雌激素 (8.59pg/ml± 3.0 1 pg/ml)明显升高 (P<0 .0 1 ) ,2 4 h尿钙、尿钙与肌酐比值降低 ,2 4 h尿羟脯氨酸升高 ,与手术组比较有显著差异 (P<0 .0 5)。结论 卵巢切除后 ,雌激素的降低和 AGEs的增加是导致骨质疏松的主要原因。而氨基胍通过降低体内
Objective Exploring the role of advanced glycosylation end products in the pathogenesis of ovariectomy-induced osteoporosis and prevention and treatment for ovariectomy-induced osteoporosis with aminoguanidine. Methods 10 months rats were ovariectomized to induce osteoporosis in this study.Determining bone mineral density, contents of AGEs from bone collagen,biochemical indexes in serum and urine which related to bone metabolism.Results Contents of AGE from ovariectomized rats' bone collagen (59.86RU/mg collagen±3.13 RU/mg collagen) were higher than that from sham group(53.83 RU/mg collagen ±5.46 RU/mg collagen) (P<0.01).Bone mineral density(0.207g/crn2±0. 010 g/crn2) were significantly reduced in the ovariectomized rats compared with that in sham group (0.236 g/ crn2±0.017 g/ crn2) (P<0.01).Levels of Serum estrogen (4.50pg/ml±1.73pg/ml) in ovariectomized rats had a decrease compared with that in sham group (8.45pg/ml±2.90pg/ml ) (P<0.02). Levels of Ca/Cr, contents of Ca, Levels of P/Cr, contents of P in ovariectomized rats' urine have an increased tendency. Tibia bone mineral density (0.221 g/ crn2±0.017 g/ crn2) from the ovariectomized rats given with aminoguanidine was higher compared with that in ovariectomized rats (P<0.05). Contents of AGEs(51.23 RU/mg collagen±7.46 RU/mg collagen) from bone collagen in ovariectomized rats given with aminoguanidine were lower than that from ovariectomized rats (P<0.01). Levels of Serum estrogen (8.59pg/ml±3.01pg/ml ) in ovariectomized rats given with aminoguanidine had an increase compared with that in ovariectomized rats (P<0.01). Levels of Ca/Cr, contents of Ca, contents of HOP from urine in ovariectomized rats given with aminoguanidine remarkably decreased compared with that in ovariectomized rats.Conclusions Increased AGEs contents from bone collagen in ovariectomized rats and decreased serum estrogen levels resulted in the reduced bone formation absolutely and the increased bone resorption relatively by multiplex ways. Which was responsible for the pathogenesis of postmenopausal osteoporosis and Aminoguanidine can prevent ovariectomized rat from bone loss by repressing the AGE production.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2003年第1期40-42,共3页
Chinese Journal of Gerontology
关键词
晚期糖化终末产物
去卵巢大鼠
骨质疏松
绝经
氨基胍
Advanced glycosylation end products Ovariectomy Osteoporosis Bone mineral density Estrogen
