Bone cancer pain model in mice: evaluation of pain behavior, bone destruction and morphine sensitivity
Bone cancer pain model in mice: evaluation of pain behavior, bone destruction and morphine sensitivity
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DOI：
10.1016/j.pbb.2004.07.011
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发表时间：
2004-10-01
影响因子：
3.6
通讯作者：
Meert, TF
中科院分区：
文献类型：
--
作者：
Vermeirsch, H;Nuydens, RM;Meert, TF
该研究的主要目的是将骨癌生长过程中的疼痛发展与客观获得的肿瘤引起的骨形态变化相关联。此外，还评估了这种骨痛对吗啡的敏感性。将溶骨性NCTC2472细胞注射到小鼠股骨中，并在3周的时间内对其行为进行观察。在观察期间，观察到荷瘤动物的疼痛行为增加。患肿瘤的小鼠表现出自发性和运动诱发的抬腿行为，后者是通过对肿瘤进行无害触诊诱发的。到第23天，在转棒上强制行走时患病肢体的使用减少到几乎完全不用。在第23天，对荷瘤骨骼进行微型计算机断层扫描以评估骨破坏情况。不同的指示骨溶解或骨折的骨参数与疼痛行为显著相关。在另一组小鼠中，在肿瘤生长的第17天和第21天评估了不同吗啡剂量对疼痛行为的影响。自发性抬腿和运动诱发的抬腿对吗啡治疗敏感，尽管由于反复约束导致的应激性镇痛可能会使小鼠运动诱发的抬腿行为最小化。高剂量吗啡仅略微改善了强制行走时肢体的使用情况。（C）2004爱思唯尔公司。保留所有权利。
The primary aim of the study was to correlate pain development during bone cancer growth with objectively obtained tumor-induced changes in bone morphology. Additionally morphine sensitivity of this bone pain was evaluated. Mice were injected into the femur with osteolytic NCTC2472 cells, and behaviorally followed during a 3-week period. During the observation period increasing pain behavior was observed in tumor-bearing animals. Tumor mice exhibited spontaneous and movement-evoked lifting, the latter evoked through non-noxious palpation of the tumor. Limb use during forced ambulation on a rotarod decreased to substantial non-use of the affected limb by day 23. On day 23, micro-computer tomography scans of the tumor-bearing bones were evaluated for bone destruction. Different bone parameters indicative of osteolysis or fragmentation were significantly correlated with pain behavior. In a separate group of mice the effects of different morphine doses on pain behavior were evaluated on days 17 and 21 of tumor growth. Spontaneous lifting and movement-evoked lifting were sensitive to morphine treatment, although stress-induced analgesia due to repeated restraint might minimize movement-evoked lifting in mice. Limb use during forced ambulation was only slightly ameliorated by high morphine doses. (C) 2004 Elsevier Inc. All rights reserved.