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首页> 外文期刊>Biochemical Pharmacology >The imidazoline I-2 receptor agonist 2-BFI attenuates hypersensitivity and spinal neuroinflammation in a rat model of neuropathic pain
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The imidazoline I-2 receptor agonist 2-BFI attenuates hypersensitivity and spinal neuroinflammation in a rat model of neuropathic pain

机译：咪唑啉I-2受体激动剂2-BFI在大鼠神经病疼痛模型中衰减过敏和脊髓神经炎症

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Chronic pain is a large, unmet public health problem. Recent studies have demonstrated the importance of neuroinflammation in the establishment and maintenance of chronic pain. However, pharmacotherapies that reduce neuroinflammation have not been successfully developed to treat chronic pain thus far. Several preclinical studies have established imidazoline 12 receptor (I2R) agonists as novel candidates for chronic pain therapies, and while some I2R ligands appear to modulate neuroinflammation in certain scenarios, whether they exert anti-neuroinflanunatory effects in models of chronic pain is unknown. This study examined the effects of the prototypical I2R agonist 2-(2-benzofuranyl)-2-imidazoline hydrochloride (2-BFI) on hypersensitivity and neuroinflammation induced by chronic constriction injury (CCI), a neuropathic pain model in rats. In CCI rats, twice-daily treatment with 10 mg/kg 2-BFI for seven days consistently increased mechanical and thermal nociception thresholds, reduced GFAP and Iba-1 levels in the dorsal horn of the spinal cord, and reduced levels of TNF-alpha relative to saline treatment. These results were recapitulated in primary mouse cortical astrocyte cultures. Incubation with 2-BFI attenuated GFAP expression and supernatant TNF-alpha levels in LPS-stimulated cultures. These results suggest that I2R agonists such as 2-BFI may reduce neuroinflammation which may partially account for their antinociceptive effects.
机译：慢性疼痛是一个大，未满足的公共卫生问题。最近的研究表明神经炎症在慢性疼痛的建立和维持中的重要性。然而，减少神经炎性炎症的药物治疗尚未成功地发展到目前为止治疗慢性疼痛。几项临床前研究已经建立了咪唑啉12个受体（I2R）激动剂作为用于慢性疼痛疗法的新候选者，而一些I2R配体似乎在某些情况下调节神经炎症，但它们是否在慢性疼痛模型中施加抗神经胰管作用是未知的。该研究检测了原型I2R激动剂2-（2-苯并呋喃基）-2-咪唑啉盐酸盐（2-BFI）对慢性收缩损伤（CCI）诱导的对大鼠神经性疼痛模型诱导的超敏反应和神经炎性的影响。在CCI大鼠中，用10mg / kg 2-bfi两次治疗七天，始终增加了脊髓背角的机械和热伤害阈值，减少了GFAP和IBA-1水平，降低了TNF-α的水平降低相对于盐水处理。这些结果在原发性小鼠皮质星形胶质细胞培养物中综合。孵育与2-BFI衰减的GFAP表达和LPS刺激培养物中的上清液TNF-α水平。这些结果表明，2-BFI等I2R激动剂可以减少神经炎症，这可能部分地占他们的抗伤害效应。

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