氧化应激与大鼠增龄性骨量减少关系的初步探究

目的探讨氧化应激与大鼠增龄性骨量减少之间的关系,为老年性骨质疏松症的临床干预提供理论依据。方法选用2、6及18月龄Wistar大鼠各20只,按月龄分为幼年、中年、老年3组,采用比色法检测血清中氧化指标晚期氧化蛋白产物(AOPP)、丙二醛(MDA)、一氧化氮(NO)含量和抗氧化指标超氧化物歧化酶(SOD)活力,并用双光子骨密度仪测定大鼠离体股骨骨密度值。结果(1)与幼年组、青年组相比,老年组骨密度显著降低(P0.01),而幼年组与青年组之间无显著性差异(P0.05)。(2)老年组与幼年组、青年组比较,AOPP、MDA含量升高(P0.01),而幼年组与青年组之间无显著性差异(P0.05),SOD活力则显示随年龄的增加而下降(P0.05),各组之间NO含量差异无显著性(P0.05);(3)股骨骨密度与AOPP含量之间呈负相关关系(r=-0.640;P0.01);与MDA含量负相关(r=-0.421;P0.01),与SOD活力正相关(r=0.483;P0.01),与NO含量无相关性(r=-0.246;P0.05)。结论随着大鼠年龄的增加,骨量逐渐减少,机体内的氧化应激水平逐渐增高,提示氧化应激与大鼠增龄性骨量减少关系密切。

The relationship between oxidative stress and age-related osteopenia in rats

Objective To explore the relationship between oxidative stress and age-related osteopenia of rats,and to provide the theoretic basis for the intervention of age-related osteoporosis.Methods The colorimetry was adopted to measure the serum levels of AOPP,MDA,NO and SOD for Wistar rats at 2,6 and 18 months old (n = 20 in each group).The BMD in femur was measured by Dual-energy X-ray absorptiometry (DEXA).Results (1) The BMD in femur was decreased significantly in 18 months old rats compared with 2 and 6 months old groups (P ＜0.01),but it was not significantly different between 2 and 6 months old groups (P ＞ 0.05).(2) The serum levels of AOPP,MDA were increased significantly in 18 months old rats compared with 2 and 6 months old ones (P ＜0.01),but they were not significantly different between 2 and 6 months old groups (P ＞ 0.05).The secrum level of NO was not significantly different among 3 groups (P ＞ 0.05).The activity of SOD showed a decrease with aging (P ＜ 0.05).(3) There was a negative correlation between AOPP and femur BMD levels (r=-0.640;P ＜ 0.01).The same trend was observed between MDA and femur BMD (r=-0.421;P＜0.01).There was no correlation between NO levels and femur BMD levels(r=-0.246;P＞0.05).A positive correlation was observed between SOD and femur BMD levels (r=0.483;P＜0.01).Conclusions Increased level of oxidative stress is involved into age-related osteopenia in rats.Oxidative stress might play an important role in the pathophysiology of agerelated osteoporosis.