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目的 :评价补肾活血液延缓雄性大鼠骨衰老的作用。方法 :4 0只SD雄性大鼠随机分为 4组 ,每组 10只。分别作为 2 4月龄本底对照组、2 7月龄增龄对照组、补肾活血液低剂量组和补肾活血液高剂量组 ,增龄对照组不做任何处理 ,低剂量组、高剂量组均自 2 4月龄给药至 2 7月龄。进行相应处理后分别测定各组大鼠全身骨矿物密度(GBMD)、右侧股骨抗弯强度 (FBS)和血清骨钙素 (BGP)、尿羟脯氨酸 (U -Hyp)与肌苷 (U -Cr)。结果 :补肾活血液高剂量组的GBMD及FBS均高于 2 7月龄增龄对照组和补肾活血液低剂量组 ,但低于 2 4月龄本底对照组 ;高剂量组的BGP明显高于增龄对照组 (P <0 0 5 ) ,U -Hyp/Cr明显低于增龄对照组 (P <0 0 5 ) ,都与本底对照组相接近 ;低剂量组的BGP低于本底对照组 (P <0 0 5 ) ,U -Hyp/Cr明显高于本底对照组 (P <0 0 5 ) ,都与增龄对照组相接近。结论 :补肾活血液具有剂量依赖性地降低全身BMD的增龄性减少率和股骨抗弯强度的增龄性降低率 ,而延缓雄性大鼠增龄性骨质疏松的作用。
Objective: To evaluate the effect of Bushen Huoxue blood on delaying bone senescence in male rats. Methods: Forty male SD rats were randomly divided into 4 groups, 10 in each group. As the 24-month-old background control group, the 27-month-old age-advanced control group, the Bushenhuoxue low-dose group, and the Bushen Huoxuezhong high-dose group, the aging-aged control group did not undergo any treatment. The low-dose group and the high-dose group All were dosed from 24 months to 27 months of age. The corresponding systemic bone mineral density (GBMD), right femur bending strength (FBS) and serum osteocalcin (BGP), urinary hydroxyproline (U-Hyp) and inosine were measured after corresponding treatment. U -Cr). RESULTS: The GBMD and FBS in the high-dose Bushen Huoxue group were higher than those in the 27-year-old age-advanced control group and the Bushen Huoxue low-dose group, but were lower in the 24-year-old background control group; the BGP in the high-dose group was significantly higher. In the Yulingling control group (P <0 05), U-Hyp/Cr was significantly lower than the age-increasing control group (P <0 05), which were close to the background control group; the BGP of the low-dose group was lower than this In the bottom control group (P <0 05), U-Hyp/Cr was significantly higher than the background control group (P <0 05), and both were similar to the aged control group. Conclusion : Bushen Huoxue blood dose-dependently reduced the rate of age-related BMD decrease and age-related decline of femur bending strength, and delayed the effect of age-related osteoporosis in male rats.