摘要
目的晚期氧化蛋白质终产物(Advanced Oxidation Protein Products,AOPPs)是一种新型炎症介质,参与多种疾病的发生、发展。本研究探讨AOPPs对老年大鼠骨密度和骨微结构的影响。方法 70只18月龄雄性SD大鼠随机分为A、B、C、D、E5组,分别给予以下处理:A组,PBS液,50 mg/kg·d(静脉注射);B组,大鼠血清白蛋白溶液(RSA)50 mg/kg·d(静脉注射);C组,AOPPs修饰的RSA溶液(AOPPs-RSA)50mg/kg·d(静脉注射);D组,AOPPs-RSA 50mg/kg.d(静脉注射)+apocynin溶液(NADPH氧化酶抑制剂)100mg/kg·d(经饮水摄入);E组,apocynin 100mg/kg·d溶液(经饮水摄入)。在干预8周和16周后取动脉血、双侧胫骨、股骨和腰4(L4)椎体标本。检测血浆AOPPs浓度;测量右侧股骨及L4椎体骨密度;显微CT分析左侧胫骨及L4椎体骨微结构相关指标,包括骨小梁体积分数(BV/TV,%)、平均骨小梁厚度(Tb.Th,mm)、平均骨小梁数目(Tb.N,1/mm)、骨小梁分离度(Tb.Sp,mm)、骨小梁结构异性程度(Degree of Anisotropy,DA)及结构模型指数(Structure Model Index,SMI)。结果相对PBS组、RSA组,2个时间点下AOPPs-RSA组老年大鼠血浆AOPPs含量明显均升高;L4椎体骨密度降低,而股骨骨密度变化不大;胫骨及L4椎体BV/TV、Tb.Th减小而Tb.Sp增大,Tb.N、DA、SMI无明显变化。AOPPs-RSA所致以上效应均能被apocynin阻断。结论 AOPPs能引起老年大鼠骨量减少、骨微结构退行性改变,促进骨退化。本研究为探索老年性骨质疏松症的发生、发展机制提供了新的思路。
Objective Advanced oxidation protein products （AOPPs） is a new defined inflammatory factor and is involved in many diseases. The present study aimed to evaluate the effect of AOPPs on bone mineral density and bone microstructure in senile rats. Methods Seventy 18-month-old male Sprague Dawley （SD） rats were randomly divided to 5 groups, group A （intravenous injection of vehicle）, group B （native rat serum albumin, RSA）, group C （AOPPs-modified RSA, AOPPs-RSA）, group D （AOPPs-modified RSA with oral administration of apocynin, a NADPH oxidase inhibitor） , and group E （apocynin alone）. After the treatment for 8 weeks or 16 weeks, blood samples, the femurs, tibias, and the fourth vertebral （L4） bodies were harvested, Plasma AOPPs level was detected. Bone mineral density （BMD） of the right femur was examined and the bone microstructure parameters of the left tibia and L4 were analyzed using micro-CT, including bone volume over total volume （ BV/TV, % ） , trabecular thickness （Tb. Th, mm） , trabecular number （Tb. N, 1/mm） , trabecular separation （Tb. Sp, mm） , the degree ofanisotropy （DA）, and the structure model index （SMI）. Results Compared to PBS group or RSA group, the AOPPs-RSA group displayed significantly elevated plasma AOPPs level. BMD of L4 in AOPPs-RSA treated rats decreased markedly while there was no significant difference in their femurs. In the microstructure analysis, AOPPs-RSA treatment was associated with decrease in BV/TV and Tb. N, but increase in Tb. Sp. However, there were no significant change regarding to Tb. N, DA, and SMI. The above effects of AOPPs-RSA were occluded by apocynin. Conclusion AOPPs cause bone mass loss and bone microstructure degeneration, and accelerate bone deterioration in senile rats in vivo. These data provide new information toward understanding of the pathogenic basis of senile osteoporosis.
出处
《中国骨质疏松杂志》
CAS
CSCD
北大核心
2015年第11期1313-1317,共5页
Chinese Journal of Osteoporosis
基金
广东省科技计划项目(2013B021800144)
