Neuropathic pain is caused by somatosensory nervous system disorder which happens in patients with different diseases. Akt3 regulates innate immune function and plays a role in neuropathic pain pathogenesis in rats. MiR-20b-5p is a microRNA which has been suggested to inhibit Akt3 expression through directly targeting Akt3 mRNA. This research focused on miR-20b-5p function in neuropathic pain by Akt3 expression inhibition. Chronic constriction injury (CCI) was employed to induce neuropathic pain in rats. Paw withdrawal thresholds and paw withdrawal latency were examined to show neuropathic pain development. Expression levels of relative genes or microRNA were checked using qRT-PCR and western blot. Inflammation cytokine levels were measured by enzyme-linked immunosorbent assay kits. In CCI rat model, miR-20b-5p level was declined and Akt3 mRNA level was upregulated. MiR-20b-5p mimics suppressed the enhanced neuropathic pain, neuroinflammation, and Akt3 expression. MiR-20b-5p directly targeted Akt3 mRNA and downregulated the Akt3 expression in rat primary microglial cells. MiR-20b-5p inhibitory function in neuropathic pain was suppressed by the upregulation of Akt3 expression. This research illustrated that miR-20b-5p alleviated neuropathic pain through the inhibition of Akt3 expression in CCI rat model.

中文翻译：

---

MiR-20b-5p通过靶向Akt3在慢性收缩性损伤大鼠模型中缓解神经性疼痛。

神经性疼痛是由躯体感觉神经系统疾病引起的，这种疾病发生在患有不同疾病的患者中。Akt3调节先天免疫功能，并在大鼠神经性疼痛发病机理中起作用。MiR-20b-5p是一种microRNA，已建议通过直接靶向Akt3 mRNA来抑制Akt3表达。这项研究集中于通过Akt3表达抑制在神经性疼痛中的miR-20b-5p功能。慢性收缩损伤（CCI）用于诱导大鼠神经性疼痛。检查爪退缩阈值和爪退缩潜伏期以显示神经性疼痛的发展。使用qRT-PCR和Western blot检测相关基因或microRNA的表达水平。通过酶联免疫吸附测定试剂盒测量炎症细胞因子水平。在CCI大鼠模型中 miR-20b-5p水平下降，Akt3 mRNA水平上调。MiR-20b-5p模拟物抑制了神经性疼痛，神经炎症和Akt3表达的增强。MiR-20b-5p直接靶向Akt3 mRNA，并下调大鼠原代小胶质细胞中Akt3的表达。ARK3表达上调抑制了MiR-20b-5p在神经性疼痛中的抑制功能。这项研究表明，miR-20b-5p通过抑制CCI大鼠模型中的Akt3表达来减轻神经性疼痛。