Neuropathic pain is a most challenging diseases worldwide, caused by the injury of nerve system. Circular RNAs (circRNAs) are revealed to be involved in various diseases, including neuropathic pain. However, the way circRNAs participate in the progress of neuropathic pain still needs further study. Identifying the possible circRNA expression patterns of neuropathic pain is of great significance to understand its underlying mechanism. Previously, circ_0005075 has been regarded as an important oncogene in multiple cancers and it has been characterized as an inflammation‑associated circRNA in various processes. Nevertheless, the functional role of circ_0005075 in neuropathic pain development is still poorly known. In our present study, we observed circ_0005075 was obviously increased in CCI rat models. Knockdown of circ_0005075 repressed the behaviors of neuropathic pain including mechanical and thermal hyperalgesia. Moreover, loss of circ_0005075 could repress the neuroinflammation via targeting COX-2, IL-6 and TNF-α whereas inducing IL-10 in vivo. Additionally, we predicted miR-151a-3p as the potential target of circ_0005075 using bioinformatics analysis. We displayed that miR-151a-3p was greatly reduced in CCI rats and circ_0005075 reversed the repressive effect of miR-151a-3p on neuropathic pain. For another, NOTCH2 has been shown to induce a variety of intracellular responses correlated with neuropathic pain. Here, we found NOTCH2 expression was strongly induced in CCI rats and miR-151a-3p. In addition, circ_0005075 significantly rescued NOTCH2 expression, which could be repressed by miR-151a-3p. To sum up, we indicated that loss of circ_0005075 relieved neuropathic pain progression by inducement of miR-151a-3p and inactivation of NOTCH2 signaling.

神经性疼痛是由神经系统损伤引起的全球最具挑战性的疾病。环状RNA（circRNA）被发现与多种疾病有关，包括神经性疼痛。但是，circRNA参与神经性疼痛进展的方式仍需进一步研究。识别神经性疼痛的可能circRNA表达模式对理解其潜在机制具有重要意义。以前，circ_0005075被认为是多种癌症中的重要致癌基因，在各种过程中其特征都是与炎症相关的circRNA。尽管如此，circ_0005075在神经性疼痛发展中的功能作用仍然知之甚少。在我们目前的研究中，我们观察到在CCI大鼠模型中circ_0005075明显增加。敲除circ_0005075可抑制神经性疼痛的行为，包括机械性和热痛觉过敏。此外，circ_0005075的缺失可通过靶向COX-2，IL-6和TNF-α抑制神经炎症，而在体内诱导IL-10。此外，我们使用生物信息学分析将miR-151a-3p预测为circ_0005075的潜在靶标。我们显示，miR-151a-3p在CCI大鼠中大大降低，circ_0005075逆转了miR-151a-3p对神经性疼痛的抑制作用。另一方面，NOTCH2已显示出诱导多种与神经性疼痛相关的细胞内反应的能力。在这里，我们发现在CCI大鼠和miR-151a-3p中强烈诱导了NOTCH2表达。另外，circ_0005075可以显着挽救NOTCH2表达，而miR-151a-3p可能会抑制该表达。总结一下，