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吡格列酮可减轻外周神经损伤小鼠的触觉异常性疼痛和热痛觉过敏。

Pioglitazone attenuates tactile allodynia and thermal hyperalgesia in mice subjected to peripheral nerve injury.

作者信息

Maeda Takehiko, Kiguchi Norikazu, Kobayashi Yuka, Ozaki Masanobu, Kishioka Shiroh

机构信息

Department of Pharmacology, Wakayama Medical University, Wakayama, Japan.

出版信息

J Pharmacol Sci. 2008 Nov;108(3):341-7. doi: 10.1254/jphs.08207fp. Epub 2008 Nov 13.

Abstract

To clarify the role of peroxisome proliferator activated receptor gamma (PPARgamma) in neuropathic pain, we examined the effect of pioglitazone, a PPARgamma agonist, on tactile allodynia and thermal hyperalgesia in a neuropathic pain model. Mice were subjected to partial sciatic nerve ligation (PSL) and given pioglitazone (1 - 25 mg/kg, p.o.) once daily. PPARgamma was distributed in the neurons of the dorsal root ganglion and the dorsal horn of the spinal cord and in the adipocytes at the epineurium of the sciatic nerve in naive mice. PSL elicited tactile allodynia and thermal hyperalgesia for two weeks. Administration of pioglitazone for the first week after PSL attenuated thermal hyperalgesia and tactile allodynia, which was dose-dependent and blocked by GW9662 (2 mg/kg, i.p.), a PPARgamma antagonist. Administration of pioglitazone for the second week also relieved tactile allodynia, but administration one week before PSL had no effect. A single administration of pioglitazone to mice on day 7 of PSL did not alter tactile allodynia and thermal hyperalgesia. PSL-induced upregulation of tumor necrosis factor-alpha and interleukin-6, which are essential for neuropathic pain, was suppressed by pioglitazone for the first week. This suggests that pioglitazone alleviates neuropathic pain through attenuation of proinflammatory cytokine upregulation by PPARgamma stimulation.

摘要

为阐明过氧化物酶体增殖物激活受体γ(PPARγ)在神经性疼痛中的作用,我们在神经性疼痛模型中研究了PPARγ激动剂吡格列酮对触觉异常性疼痛和热痛觉过敏的影响。将小鼠进行坐骨神经部分结扎(PSL),并每天一次给予吡格列酮(1 - 25毫克/千克,口服)。在未处理的小鼠中,PPARγ分布于背根神经节和脊髓背角的神经元以及坐骨神经外膜的脂肪细胞中。PSL诱发了两周的触觉异常性疼痛和热痛觉过敏。在PSL后第一周给予吡格列酮可减轻热痛觉过敏和触觉异常性疼痛,呈剂量依赖性,并被PPARγ拮抗剂GW9662(2毫克/千克,腹腔注射)阻断。在PSL后第二周给予吡格列酮也可缓解触觉异常性疼痛,但在PSL前一周给药则无效。在PSL第7天对小鼠单次给予吡格列酮并未改变触觉异常性疼痛和热痛觉过敏。吡格列酮在第一周抑制了PSL诱导的肿瘤坏死因子-α和白细胞介素-6的上调,这两种细胞因子对神经性疼痛至关重要。这表明吡格列酮通过刺激PPARγ减轻促炎细胞因子上调来缓解神经性疼痛。

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