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目的探讨长期尼古丁摄入对大鼠骨内微结构、骨生物力学性能以及氧化应激状态的影响。方法取6周龄雄性SD大鼠36只,体质量160~180 g,随机分为3组,分别为对照组、低剂量组和高剂量组,每组12只。高剂量组和低剂量组分别按照每天6.0、0.4 mg/kg标准尼古丁灌胃干预,持续12个月;对照组不作处理。实验期间观察各组大鼠存活情况,每个月大鼠称重。造模12个月后处死全部大鼠,取L1椎体进行Micro-CT三维重建测量骨密度(bone mineral density,BMD)、骨体积分数(bone volume fraction,BVF)、骨小梁厚度(trabecular thickness,TT)、骨小梁数目(trabecular number,TN)、骨小梁间隙(trabecular spacing,TS),取左侧股骨干进行生物力学测试最大载荷、抗弯刚度、最大断裂能;取动脉血检测丙二醛(malonyldialdehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)、过氧化氢酶(catalase,CAT)以及可替宁含量。结果实验期间,高剂量组死亡2只大鼠,低剂量组死亡1只,对照组大鼠均存活。随时间延长,高、低剂量组大鼠体质量逐渐低于对照组,8~12个月时,高、低剂量组与对照组比较差异有统计学意义(P<0.05);11、12个月时,高剂量组大鼠体质量明显低于低剂量组(P<0.05)。造模12个月后,高剂量组BMD、BVF、TT、TN均显著低于对照组、低剂量组,TS显著增高(P<0.05);低剂量组仅BVF、TN、TS与对照组比较差异有统计学意义(P<0.05)。高剂量组股骨干最大载荷、抗弯刚度以及最大断裂能明显低于对照组、低剂量组,低剂量组明显低于对照组(P<0.05)。与对照组比较,高、低剂量组可替宁以及MDA含量均明显升高,CAT、SOD含量明显降低(P<0.05);且高、低剂量组间差异亦有统计学意义(P<0.05)。结论长期尼古丁摄入会引起大鼠骨内微结构改变、骨生物力学性能下降以及氧化-抗氧化水平失衡,长期高剂量尼古丁摄入可能是导致骨质疏松症发生的原因之一。
Objective To investigate the effects of long-term nicotine intake on the intraosseous microarchitecture, bone biomechanical properties and oxidative stress in rats. Methods Thirty - six male Sprague Dawley rats aged 6 weeks were randomly divided into three groups: control group, low dose group and high dose group, with 12 rats in each group. High-dose group and low-dose group according to the daily 6.0,0.4 mg / kg standard nicotine gavage intervention for 12 months; the control group without treatment. Survival of rats in each group was observed during the experiment, rats were weighed every month. All the rats were sacrificed 12 months after the model establishment. The L1 vertebrae were examined by Micro-CT three-dimensional reconstruction to measure the bone mineral density (BMD), bone volume fraction (BVF), trabecular thickness , TT, trabecular number (TN), trabecular spacing (TS), maximum force of biomechanical test, flexural stiffness and maximum energy of rupture of left femoral shaft were measured. Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and cotinine content. Results During the experiment, two rats died in the high-dose group, one died in the low-dose group, and all the rats in the control group survived. Over time, the body weight of rats in high and low dose groups was gradually lower than that in control group, and there was significant difference between high and low dose groups and control group at 8 ~ 12 months (P <0.05); 11 and 12 The body weight of rats in high dose group was significantly lower than that in low dose group (P <0.05). After 12 months, the BMD, BVF, TT and TN of the high-dose group were significantly lower than those of the control group and the low-dose group and the TS were significantly increased (P <0.05); only the BVF, TN and TS of the low- The difference was statistically significant (P <0.05). The maximum load, flexural rigidity and maximum fracture energy of femoral shaft in high dose group were significantly lower than those in control group, while those in low dose group and low dose group were significantly lower than those in control group (P <0.05). Compared with the control group, the cotinine and MDA levels in the high and low dose groups were significantly increased, while the contents of CAT and SOD were significantly decreased (P <0.05), and the difference between the high and low dose groups was also statistically significant (P <0.05 ). Conclusion Long-term nicotine ingestion induces changes of intraosseous microstructure, decreased biomechanical properties and imbalance of oxidation-anti-oxidation in rats. Long-term high-dose nicotine intake may be one of the reasons leading to osteoporosis.