Department of Spinal Surgery, Henan Provincial People's Hospital, People's Hospital, of Zhengzhou University, Zhengzhou, Henan, China.
Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12034-12040. doi: 10.26355/eurrev_202012_23992.
Neuropathic pain (NP) is one of the most intractable complications of spinal cord injury (SCI). This study aims to explore the role of long non-coding RNA (lncRNA) SNHG1 in influencing SCI-induced NP.
After establishment of the spinal nerve ligation (SNL) model in rats, spinal tissues were extracted. SNHG1 level in rat spinal tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The role of SNHG1 in the development of NP was explored by assessing paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) in model rats. The interaction between SNHG1 and CDK4 was explored by Luciferase assay and RIP (RNA-Binding Protein Immunoprecipitation). Enzyme-linked immunosorbent assay (ELISA) and qRT-PCR were conducted to determine inflammatory factor levels in rat spinal tissues.
SNHG1 was upregulated in rats undergoing SNL. Knockdown of SNHG1 alleviated the development of NP and overexpression of SNHG1 was capable of inducing NP symptoms in uninjured rats. SNHG1 induced NP by directly regulating CDK4 level.
SNHG1 is a novel target in the treatment of NP associated with neuroinflammation.
神经性疼痛（NP）是脊髓损伤（SCI）最棘手的并发症之一。本研究旨在探讨长链非编码 RNA（lncRNA）SNHG1 在影响 SCI 诱导的 NP 中的作用。
建立大鼠脊神经结扎（SNL）模型后，提取脊髓组织。采用实时定量聚合酶链反应（qRT-PCR）检测大鼠脊髓组织中 SNHG1 水平。通过评估模型大鼠的足底退缩阈值（PWT）和足底退缩潜伏期（PWL），探讨 SNHG1 在 NP 发展中的作用。通过荧光素酶测定和 RIP（RNA 结合蛋白免疫沉淀）探索 SNHG1 与 CDK4 的相互作用。采用酶联免疫吸附试验（ELISA）和 qRT-PCR 检测大鼠脊髓组织中炎症因子水平。
SNL 后大鼠 SNHG1 上调。SNHG1 敲低减轻了 NP 的发展，而过表达 SNHG1 可在未受伤的大鼠中诱导 NP 症状。SNHG1 通过直接调节 CDK4 水平诱导 NP。
SNHG1 是治疗神经炎症相关 NP 的一个新靶点。
