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首页> 外文期刊>The journal of pain: official journal of the American Pain Society >A Kappa Opioid Receptor Agonist Blocks Bone Cancer Pain Without Altering Bone Loss, Tumor Size, or Cancer Cell Proliferation in a Mouse Model of Cancer-Induced Bone Pain
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A Kappa Opioid Receptor Agonist Blocks Bone Cancer Pain Without Altering Bone Loss, Tumor Size, or Cancer Cell Proliferation in a Mouse Model of Cancer-Induced Bone Pain

机译：Kappa阿片受体激动剂阻断骨癌疼痛而不改变癌症诱导的骨疼痛的小鼠模型中的骨质损失，肿瘤大小或癌细胞增殖

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摘要

Breast cancer metastasizes to bone, diminishing quality of life of patients because of pain, fracture, and limited mobility. Cancer-induced bone pain (CIBP) is characterized as moderate to severe ongoing pain, primarily managed by mu opioid agonists such as fentanyl. However, opioids are limited by escalating doses and serious side effects. One alternative may be kappa opioid receptor (KOR) agonists. There are few studies examining KOR efficacy on CIBP, whereas KOR agonists are efficacious in peripheral and inflammatory pain. We thus examined the effects of the KOR agonist U50,488 given twice daily across 7 days to block CIBP, tumor-induced bone loss, and tumor burden. U50,488 dose-dependently blocked tumor-induced spontaneous flinching and impaired limb use, without changing tactile hypersensitivity, and was fully reversed by the KOR antagonist nor-binaltorphimine. U50,488 treatment was higher in efficacy and duration of action at later time points. U50,488 blocked this pain without altering tumor-induced bone loss or tumor growth. Follow-up studies in human cancer cell lines confirmed that KOR agonists do not affect cancer cell proliferation. These studies suggest that KOR agonists could be a new target for cancer pain management that does not induce cancer cell proliferation or alter bone loss.
机译：乳腺癌转移到骨骼，由于疼痛，骨折和有限的流动性，患者的生活质量减少。癌症诱导的骨疼痛（CIBP）的特征是中度至严重的持续疼痛，主要由Mu阿片类Agonist等芬太尼管理。然而，阿片类药物通过升级剂量和严重副作用而受到限制。一种替代方案可以是κ阿片类受体（Kor）激动剂。少量研究kor对cibp的疗效研究，而Kor激动剂在外周和炎症疼痛中是有效的。因此，我们检查了每天两次给予的Kor激动剂U50,488的影响，以阻止CIBP，肿瘤诱导的骨质损失和肿瘤负担。 U50,488剂量依赖性阻断肿瘤诱导的自发性甩出和损伤的肢体使用，而不会改变触感超敏反应，并由KOR拮抗剂NOR-BINARTORERHIMINE完全逆转。 u50,488治疗效果高，在稍后的时间点的作用持续时间较高。 U50,488堵塞这种疼痛而不改变肿瘤诱导的骨质损失或肿瘤生长。人癌细胞系中的后续研究证实kor激动剂不会影响癌细胞增殖。这些研究表明，Kor激动剂可能是癌症疼痛管理的新靶，不会诱导癌细胞增殖或改变骨质损失。

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