INTRODUCTION The polarization state of microglia affects the progress of neuropathic pain. MiR-155 modulates polarization of microglia, while its role in neuropathic pain has not been well studied. MATERIAL AND METHODS We separately used lipopolysaccharide (LPS) and interleukin 4 (IL-4) for constructing an M1/M2 polarization model in BV-2 cells. The levels of CD86, iNOS, CD206, Arg and miR-155 were measured by western blot or qRT-PCR, as needed. Subsequently, BV-2 cells were transfected with miR-155 mimics or inhibitor to explore the effects of miR-155 on polarization states. We also constructed a neuropathic pain model by applying spinal nerve ligation (SNL) in Wistar rats with miR-155 agomir or antagomir injection. The withdrawal threshold was measured by Von Frey fibre needle. The levels of interleukin 1b (IL-1b), tumour necrosis factor a (TNF-a) and the proportion of M1-polarized microglia in primary microglia from rats were measured by ELISA and flow cytometry. RESULTS LPS induced M1 polarization in BV-2 cells with increasing of CD86, iNOS and miR-155, while IL-4 induced M2 polarization in BV-2 cells with increasing of CD206, Arg and decreasing of miR-155. MiR-155 mimics upregulated CD86 and downregulated CD206, whereas miR-155 inhibitor downregulated CD86 and upregulated CD206. MiR-155 antagomir increased the withdrawal threshold, decreased the production of IL-1b, TNF-a and the proportion of M1-polarized microglia in primary microglia. CONCLUSIONS Results demonstrate that suppression of miR-155 attenuates neuropathic pain by inducing an M1 to M2 switch in microglia. Our findings provide a new perspective to understand the function of miR-155 in microglia.

中文翻译：

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miR-155的抑制通过在小胶质细胞中诱导从M1到M2的切换而减轻了神经性疼痛。

简介小胶质细胞的极化状态影响神经性疼痛的进展。MiR-155调节小胶质细胞的极化，而其在神经性疼痛中的作用尚未得到充分研究。材料与方法我们分别使用脂多糖（LPS）和白介素4（IL-4）在BV-2细胞中构建M1 / M2极化模型。根据需要，通过蛋白质印迹或qRT-PCR测量CD86，iNOS，CD206，Arg和miR-155的水平。随后，用miR-155模拟物或抑制剂转染BV-2细胞，以探索miR-155对极化状态的影响。我们还通过在mistar-155agomir或antagomir注射的Wistar大鼠中应用脊髓神经结扎（SNL），构建了神经性疼痛模型。通过Von Frey纤维针测量退出阈值。白细胞介素1b（IL-1b）的水平 用ELISA和流式细胞术检测大鼠的肿瘤坏死因子a（TNF-a）和原发性小胶质细胞中M1极化的小胶质细胞的比例。结果LPS诱导BV-2细胞M1极化随CD86，iNOS和miR-155的增加，而IL-4诱导BV-2细胞M2极化随CD206，Arg的增加和miR-155的减少。MiR-155模拟上调CD86和下调CD206，而miR-155抑制剂下调CD86和上调CD206。MiR-155 antagomir增加了戒断阈值，降低了IL-1b，TNF-a的产生以及原发性小胶质细胞中M1极化小胶质细胞的比例。结论结果表明，miR-155的抑制通过在小胶质细胞中诱导M1至M2转换而减轻了神经性疼痛。