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首页> 外文期刊>Journal of Cellular Physiology >NEAT1 contributes to neuropathic pain development through targeting miR‐381/HMGB1 axis in CCI rat models
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NEAT1 contributes to neuropathic pain development through targeting miR‐381/HMGB1 axis in CCI rat models

机译:NEAT1导致神经性疼痛的发展通过针对miR量381 / HMGB1轴CCI老鼠模型

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LncRNAs have been recognized as significant regulators in various diseases including neuropathic pain. Although the lncRNA NEAT1 has been reported to be involved in multiple cancers, its biological functions in neuropathic pain still remain unknown. In our present study, a chronic constriction injury (CCI) rat model was established and we found that NEAT1 was greatly upregulated in the spinal cord tissues of CCI rats. Knockdown of NEAT1 can repress neuropathic pain behaviors including mechanical and thermal hyperalgesia. In addition, NEAT1 downregulation inhibited neuroinflammation via inhibiting IL‐6, IL‐1β, and tumor necrosis factor (TNF)‐α in CCI rats. We also observed that miR‐381 was decreased significantly in CCI rats. By using bioinformatics analysis, miR‐381 was predicted to be a microRNA target of NEAT1, which indicated a negative correlation between miR‐381 and NEAT1. Inhibition of NEAT1 can induce miR‐381 expression in CCI rats, which indicated a negative correlation between NEAT1 and miR‐381. HMGB1, as a downstream target gene of miR‐381 was observed to be dramatically increased in CCI rats. miR‐381 can modulate HMGB1 expression negatively and meanwhile, NEAT1 was able to regulate HMGB1 through sponging miR‐381. Downregulation of HMGB1 can inhibit neuropathic pain behaviors which can be reversed by miR‐381 inhibitors. Taken these together, it was indicated that NEAT1 can induce neuropathic pain development in CCI rats via regulating miR‐381/HMGB1 axis.
机译:LncRNAs被认为是重要的在各种疾病,包括监管机构神经性疼痛。被报道参与多个癌症,神经性疼痛的生物功能仍然是未知的。慢性收缩损伤(CCI)大鼠模型建立和我们发现NEAT1是极大的调节脊髓组织的CCI老鼠。疼痛行为包括机械和热痛觉过敏。通过抑制神经炎症抑制IL高6IL 1β,应承担和肿瘤坏死因子(TNF)在CCIα老鼠。老鼠在CCI显著。生物信息学分析,米尔381年预言microRNA NEAT1的目标,这表明米尔381和NEAT1应承担的负相关关系。抑制NEAT1还可以诱导米尔381表达式CCI老鼠,表示负数381年NEAT1之间的相关性和米尔。下游靶基因的米尔381年观察到的老鼠在CCI大幅度增加。可以调节HMGB1表达消极和与此同时,NEAT1能够调节HMGB1通过骗取米尔381。可以抑制神经性疼痛行为可以吗381年被逆转,米尔的抑制剂。在一起,这是表明NEAT1可以诱导神经性疼痛发展CCI老鼠通过调节米尔381 / HMGB1轴。

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