BACKGROUND Diabetic neuropathy is a serious complication for diabetic patients involving the nervous system. This disease is a quiet but painful condition caused by chronically high blood glucose levels. It is reported that high mobility group box 1 protein (HMGB1) participates in the development of neuropathic pain. This study aimed to explore the role of microRNA (miR)-193a in diabetic neuropathic pain through the regulation of HMGB1. METHODS A diabetic mouse model was established through the injection of streptozocin (STZ). Neuropathic pain development was shown by paw withdrawal thresholds and paw withdrawal latency. Expression levels of relative genes or miR were analyzed by qRT-PCR, while Western blot was employed to assess the protein levels. The interaction between miR-193a and HMGB1 mRNA 3'-UTR region was shown by luciferase assay. The levels of inflammation cytokines were measured by ELISA kits. RESULTS miR-193a expression was decreased and HMGB1 expression was upregulated in the lumbar spinal dorsal horn of STZ-induced diabetic mice. miR-193a inhibited HMGB1 expression in the lumbar spinal dorsal horn. Overexpression of miR-193a alleviated neuropathic pain in STZ-induced diabetic mice. Peripheral neuroinflammation in diabetic mice was suppressed by miR-193a overexpression. CONCLUSION This research illustrates that miR-193a alleviates diabetic neuropathic pain in a mouse model through the inhibition of HMGB1 expression.

中文翻译：

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MicroRNA-193a下调HMGB1以减轻小鼠模型中的糖尿病性神经性疼痛。

背景技术对于涉及神经系统的糖尿病患者，糖尿病性神经病是严重的并发症。这种疾病是一种由慢性高血糖引起的安静但痛苦的疾病。据报道，高迁移率族盒1蛋白（HMGB1）参与神经性疼痛的发展。这项研究旨在探讨通过调控HMGB1 microRNA（miR）-193a在糖尿病性神经性疼痛中的作用。方法通过注射链脲佐菌素（STZ）建立糖尿病小鼠模型。爪退缩阈值和爪退缩潜伏期显示神经性疼痛的发展。通过qRT-PCR分析相关基因或miR的表达水平，同时采用蛋白质印迹法评估蛋白质水平。通过荧光素酶测定显示了miR-193a和HMGB1 mRNA 3'-UTR区域之间的相互作用。通过ELISA试剂盒测量炎症细胞因子的水平。结果STZ诱导的糖尿病小鼠的腰椎背角miR-193a表达降低，HMGB1表达上调。miR-193a抑制HMGB1在腰椎背角的表达。miR-193a的过表达减轻了STZ诱导的糖尿病小鼠的神经性疼痛。miR-193a过表达抑制了糖尿病小鼠的周围神经炎症。结论这项研究表明miR-193a通过抑制HMGB1表达减轻了小鼠模型中的糖尿病性神经性疼痛。miR-193a抑制HMGB1在腰椎背角的表达。miR-193a的过表达减轻了STZ诱导的糖尿病小鼠的神经性疼痛。miR-193a过表达抑制了糖尿病小鼠的周围神经炎症。结论这项研究表明miR-193a通过抑制HMGB1表达减轻了小鼠模型中的糖尿病性神经性疼痛。miR-193a抑制HMGB1在腰椎背角的表达。miR-193a的过表达减轻了STZ诱导的糖尿病小鼠的神经性疼痛。miR-193a过表达抑制了糖尿病小鼠的周围神经炎症。结论这项研究表明miR-193a通过抑制HMGB1表达减轻了小鼠模型中的糖尿病性神经性疼痛。