Objective: To explore the potential regulation mechanisms of miR-384-5p in Neuropathic pain (NP).Methods: Rat model of chronic constriction injury (CCI) was established to induce NP in vivo. NP levels were assessed using Withdrawal Threshold (PWT) and Paw Withdrawal Latency (PWL). qPCR and Western blotting were used to determine the relative expression of miR-384-5p and SCN3A. The inflammation response in spinal microglia cells was determined by ELISA assay. Immunofluorescence assay was used to demonstrate the co-localization of miR-384-5p with SCN3A in rat dorsal root ganglions (DRGs). The target genes of miR-384-5p were verified by dual-luciferase report assays.Results: In the current study, the miR-384-5p expression level was significantly downregulated in CCI rats when comparing to the sham group. In addition, miR-384-5p agomir significantly repressed mechanical allodynia and heat hyperalgesia in CCI rats. Meanwhile, the current study indicated miR-384-5p could decrease inflammation progress in spinal microglia cells incubated in lipopolysaccharide. Consistently, overexpression of miR-384-5p obviously depressed inflammation cytokine levels in CCI rats. Dual-luciferase reporter assays indicated that SCN3A is a target gene of miR-384-5p.Conclusion: miR-384-5p is a negative regulator in the development of neuropathic pain by regulating SCN3A, indicating that miR-384-5p might be a promising therapeutic target in the treatment of neuropathic pain.Abbreviations: CCI: Chronic constriction injury; ZEB1: Zinc finger E box binding protein-1; MAPK6: Mitogen-activated protein kinase 6; COX-2: cyclooxygenase-2.

中文翻译：

---

miR-384-5p通过靶向SCN3A在慢性收缩性损伤的大鼠模型中缓解神经性疼痛。

目的：探讨miR-384-5p在神经性疼痛（NP）中的潜在调控机制。方法：建立慢性压迫损伤（CCI）大鼠体内诱导NP的模型。使用戒断阈值（PWT）和爪子戒断潜伏期（PWL）评估NP水平。使用qPCR和蛋白质印迹法确定miR-384-5p和SCN3A的相对表达。通过ELISA测定确定脊髓小胶质细胞中的炎症反应。免疫荧光法用于证明miR-384-5p与SCN3A在大鼠背根神经节（DRG）中的共定位。结果：在本研究中，与假手术组相比，CCI大鼠的miR-384-5p表达水平显着下调。此外，miR-384-5p agomir可显着抑制CCI大鼠的机械性异常性疼痛和热痛觉过敏。同时，目前的研究表明，miR-384-5p可以减少脂多糖培养的脊髓小胶质细胞的炎症进程。一致地，miR-384-5p的过表达明显降低了CCI大鼠的炎症细胞因子水平。双荧光素酶报告基因检测表明SCN3A是miR-384-5p的靶基因。结论：miR-384-5p是通过调节SCN3A在神经性疼痛发生中的负调节剂，表明miR-384-5p可能是一种调控基因。缩写：CCI：慢性收缩性损伤；ZEB1：锌指E盒结合蛋白-1；MAPK6：丝裂原激活的蛋白激酶6；COX-2：环氧合酶-2。