Lane N, Maeda H, Cullen D M, Kimmel D B
Division of Rheumatology, University of California at San Francisco 94143.
Bone Miner. 1994 Jul;26(1):43-59. doi: 10.1016/s0169-6009(08)80161-4.
Temporary immobilization creates bone loss. The purpose of this investigation was to use an agent to protect the skeleton from bone loss bone during temporary immobilization. Eighty-nine 6-month-old retired breeder Sprague-Dawley female rats were used. Animals were randomly divided into six groups of equal numbers. Four groups were given drinking water from day 0, containing naproxen (100 or 200 mg/l). At day 7, half the animals in all groups had their right hindlimb immobilized. At day 49, half the immobilized rats and non-immobilized controls were sacrificed. The remaining rats were remobilized and the drug was stopped. At day 91, all remaining rats were sacrificed. Gastrocnemius and soleus muscle weights were determined. Right tibiae were analyzed for cancellous bone mass, bone structural and bone dynamic variables. At the close of immobilization, bone mass was lower in the right (immobilized) hindlimb of the immobilized group than in the non-immobilized group. Immobilized rats drinking 100 mg/l naproxen water had significantly higher bone mass in their immobilized limbs than did untreated immobilized rats, but all rats drinking 200 mg/l naproxen water had lower bone mass than controls. After 6 weeks of recovery, bone mass in the immobilized limb of untreated formerly immobilized rats improved, but remained below untreated never-immobilized rats. Formerly immobilized rats that had been treated with 100 mg/l naproxen water had normal bone mass after 6 weeks of recovery. Naproxen, an agent that mildly depresses activation frequency, prevents some of the transient bone mass and structural deterioration during temporary immobilization. Such treatment facilitates a more rapid return to normal bone mass, though not to normal structure. The more rapid recovery occurs because the difference from normal is less, not because of more rapid formation in recovering animals.
短期制动会导致骨质流失。本研究的目的是使用一种药物来保护骨骼在短期制动期间不发生骨质流失。选用89只6月龄的退役繁殖斯普拉格-道利雌性大鼠。动物被随机分为数量相等的六组。四组从第0天开始饮用含萘普生（100或200mg/L）的饮用水。在第7天，所有组中一半的动物右后肢被制动。在第49天，处死一半制动大鼠和未制动的对照大鼠。其余大鼠解除制动并停止给药。在第91天，处死所有剩余大鼠。测定腓肠肌和比目鱼肌重量。分析右侧胫骨的松质骨质量、骨结构和骨动力学变量。在制动结束时，制动组右侧（制动）后肢的骨质量低于未制动组。饮用100mg/L萘普生水的制动大鼠其制动肢体的骨质量显著高于未治疗的制动大鼠，但所有饮用200mg/L萘普生水的大鼠骨质量均低于对照组。恢复6周后，未治疗的既往制动大鼠制动肢体的骨质量有所改善，但仍低于未制动的未治疗大鼠。曾饮用100mg/L萘普生水的既往制动大鼠在恢复6周后骨质量正常。萘普生是一种轻度降低激活频率的药物，可预防短期制动期间的一些短暂骨质流失和结构恶化。这种治疗有助于更快恢复到正常骨质量，尽管结构无法恢复正常。恢复更快是因为与正常的差异更小，而不是因为恢复动物的形成更快。
