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双氯芬酸、普瑞巴林和度洛西汀治疗大鼠废用性慢性肌肉骨骼疼痛的疗效。

Therapeutic effects of diclofenac, pregabalin, and duloxetine on disuse-induced chronic musculoskeletal pain in rats.

机构信息

Department of Anatomy, Aichi Medical University, 1-1 Yazakokarimta, Nagakute, Aichi, 480-1195, Japan.

Research Center for Next-Generation Drug Development, Research Institute of Environmental Medicine, Nagoya University, Nagoya, 464-8601, Japan.

出版信息

Sci Rep. 2018 Feb 19;8(1):3311. doi: 10.1038/s41598-018-21429-3.

DOI:10.1038/s41598-018-21429-3
PMID:29459641
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5818528/
Abstract

The aim of this study was to clarify the mechanism of disuse-induced muscle hyperalgesia through the evaluation of the pharmacological behaviour of muscle hyperalgesia profiles in chronic post-cast pain (CPCP) rats with acute and chronic-phase mirror-image muscle hyperalgesia treated with diclofenac (NSAID), pregabalin (an inhibitor of Ca channel α2δ), and duloxetine (SNRI). After 2 weeks of cast immobilization, the peak cross-sectional area and muscle wet weight of the ipsilateral soleus and gastrocnemius muscles decreased more significantly in CPCP rats than in untreated rats. Histological findings revealed disuse-induced muscle atrophy in CPCP rats. The blood biochemical parameters of CPCP rats in acute and chronic phases did not differ significantly from those of untreated rats. The diclofenac and pregabalin-treated groups exhibited no improvement in acute or chronic muscle hyperalgesia. In contrast, the duloxetine-treated group exhibited an improvement in acute muscle hyperalgesia, but showed no apparent effect on chronic muscle hyperalgesia on ipsilateral or contralateral sides. However, the chronic muscle hyperalgesia was reversed by intrathecal administration of DAMGO (a μ-opioid receptor agonist). The results suggest that chronic muscle hyperalgesia in CPCP rats did not result from an inflammatory mechanism, and there is only a low probability that it's caused by a neuropathic mechanism.

摘要

本研究旨在通过评估慢性后石膏疼痛 (CPCP) 大鼠的急性和慢性镜像肌肉痛觉过敏的药物行为，阐明失用性肌肉痛觉过敏的机制。CPCP 大鼠在 2 周的石膏固定后，其同侧比目鱼肌和腓肠肌的峰值横截面积和肌肉湿重比未治疗大鼠明显减少。组织学发现 CPCP 大鼠存在废用性肌肉萎缩。急性和慢性相 CPCP 大鼠的血液生化参数与未治疗大鼠无显著差异。双氯芬酸和普瑞巴林治疗组在急性或慢性肌肉痛觉过敏方面没有改善。相比之下，度洛西汀治疗组在急性肌肉痛觉过敏方面有所改善，但对同侧或对侧的慢性肌肉痛觉过敏无明显作用。然而，鞘内给予 DAMGO（μ-阿片受体激动剂）可逆转慢性肌肉痛觉过敏。结果表明，CPCP 大鼠的慢性肌肉痛觉过敏不是由炎症机制引起的，而且由神经病理性机制引起的可能性也很低。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2e5/5818528/2ea712eb4196/41598_2018_21429_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2e5/5818528/2ea712eb4196/41598_2018_21429_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2e5/5818528/d05b75b2d50f/41598_2018_21429_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2e5/5818528/b08939a61e75/41598_2018_21429_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2e5/5818528/5e80f324ccea/41598_2018_21429_Fig3_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2e5/5818528/de80b2ffb773/41598_2018_21429_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2e5/5818528/681bba48f897/41598_2018_21429_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2e5/5818528/2ea712eb4196/41598_2018_21429_Fig7_HTML.jpg

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