Department of Anesthesiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.
Synapse. 2019 Dec;73(12):e22125. doi: 10.1002/syn.22125. Epub 2019 Sep 6.
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.
神经病理性疼痛是由感觉神经系统障碍引起的，发生在患有不同疾病的患者中。Akt3 调节固有免疫功能，在大鼠神经病理性疼痛发病机制中发挥作用。miR-20b-5p 是一种 microRNA，已被证明通过直接靶向 Akt3 mRNA 来抑制 Akt3 表达。本研究通过抑制 Akt3 表达来关注 miR-20b-5p 在神经病理性疼痛中的作用。慢性缩窄性损伤（CCI）被用于诱导大鼠的神经病理性疼痛。通过检测足底撤回阈值和足底撤回潜伏期来显示神经病理性疼痛的发展。使用 qRT-PCR 和 Western blot 检查相对基因或 microRNA 的表达水平。在 CCI 大鼠模型中，miR-20b-5p 水平下降，Akt3 mRNA 水平上调。miR-20b-5p 模拟物抑制了增强的神经病理性疼痛、神经炎症和 Akt3 表达。miR-20b-5p 在大鼠原代小胶质细胞中直接靶向 Akt3 mRNA 并下调 Akt3 表达。miR-20b-5p 在神经病理性疼痛中的抑制作用通过 Akt3 表达的上调而受到抑制。本研究表明，miR-20b-5p 通过抑制 CCI 大鼠模型中的 Akt3 表达来缓解神经病理性疼痛。
