Background. miRNA is an essential factor in neuropathic pain. However, the underlying mechanism of miRNA in neuropathic pain remains unclear. Objective. To explore the potential role of miR-223 in neuropathic pain in a mice model of chronic sciatic nerve injury. Methods. Mice were divided into the sham group, CCI group, CCI + Lenti-vector group, and CCI + Lenti-miR-223 group. Flow cytometry was used to detect the neuronal apoptosis and the proportion of M1/M2 macrophages in each group. Western blot was used to detect the protein expression levels of ASC, caspase-1, IL-1β, and IL-18 in each group. Luciferase activity assay detects the binding of miR-223 and NLRP3. Macrophage chemotaxis experiments verified the anti-inflammatory effect of miR-223 in vitro. Results. The overexpression of miR-233 significantly reduced the neuropathic pain caused by CCI and reduced the apoptosis and inflammatory factor expression. miR-223 inhibits the expression of NLRP3 by directly binding to the 3′-untranslated region. Overexpression of miR-223 reduces the protein levels of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in the spinal cord of CCI mice, increases the proportion of M2-type macrophages, and reduces the proportion of M1-type macrophages. Conclusion. miR-223 may facilitate the development of neuropathic pain in CCI mice by inhibiting NLRP3-mediated neuroinflammation.

中文翻译：

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miR-223 通过 NLRP3/IL-1β 通路抑制巨噬细胞的极化和募集以改善神经性疼痛

背景。miRNA 是神经病理性疼痛的重要因素。然而，miRNA在神经性疼痛中的潜在机制仍不清楚。目标。探讨 miR-223 在慢性坐骨神经损伤小鼠模型神经病理性疼痛中的潜在作用。方法。将小鼠分为假手术组、CCI 组、CCI + Lenti-vector 组和 CCI + Lenti-miR-223 组。流式细胞术检测各组神经元凋亡情况及M1/M2巨噬细胞比例。用Western blot法检测ASC的蛋白质表达水平，胱天蛋白酶-1，IL-1 β和每组中的 IL-18。荧光素酶活性测定检测 miR-223 和 NLRP3 的结合。巨噬细胞趋化实验验证了 miR-223 在体外的抗炎作用。结果。miR-233的过表达显着减轻了CCI引起的神经性疼痛，降低了细胞凋亡和炎症因子的表达。miR-223 通过直接结合 3'-非翻译区来抑制 NLRP3 的表达。miR-223过表达降低CCI小鼠脊髓中NLRP3、ASC、caspase-1、IL- 1β、IL-18蛋白水平，增加M2型巨噬细胞比例，降低M1比例型巨噬细胞。结论. miR-223 可能通过抑制 NLRP3 介导的神经炎症促进 CCI 小鼠神经性疼痛的发展。