JOURNAL/nrgr/04.03/01300535-202508000-00026/figure1/v/2024-09-30T120553Z/r/image-tiff 干扰素调节因子 7 在先天免疫反应中起着至关重要的作用。然而，干扰素调节因子 7 介导的信号传导是否会导致帕金森病仍不清楚。在此，我们报告干扰素调节因子 7 在 1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的帕金森病小鼠模型中显着上调，并与小胶质细胞共定位。选择性环单磷酸鸟苷单磷酸腺苷合酶抑制剂RU.521和干扰素基因刺激剂抑制剂H151均能有效抑制暴露于1-甲基-4-苯基吡啶鎓的BV2小胶质细胞中干扰素调节因子7的活化，并抑制小鼠BV2小胶质细胞向神经毒性物质的转化M1表型。此外，siRNA介导的BV2小胶质细胞中干扰素调节因子7表达的敲低降低了诱导型一氧化氮合酶、肿瘤坏死因子α、CD16、CD32和CD86的表达，并增加了抗炎标志物ARG1和YM1的表达。综上所述，我们的研究结果表明，环单磷酸鸟苷单磷酸腺苷合酶-干扰素基因刺激剂-干扰素调节因子7通路在帕金森病的发病机制中发挥着至关重要的作用。版权所有©2025版权所有：©2025神经再生研究。

JOURNAL/nrgr/04.03/01300535-202508000-00026/figure1/v/2024-09-30T120553Z/r/image-tiff Interferon regulatory factor 7 plays a crucial role in the innate immune response. However, whether interferon regulatory factor 7-mediated signaling contributes to Parkinson's disease remains unknown. Here we report that interferon regulatory factor 7 is markedly up-regulated in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of Parkinson's disease and co-localizes with microglial cells. Both the selective cyclic guanosine monophosphate adenosine monophosphate synthase inhibitor RU.521 and the stimulator of interferon genes inhibitor H151 effectively suppressed interferon regulatory factor 7 activation in BV2 microglia exposed to 1-methyl-4-phenylpyridinium and inhibited transformation of mouse BV2 microglia into the neurotoxic M1 phenotype. In addition, siRNA-mediated knockdown of interferon regulatory factor 7 expression in BV2 microglia reduced the expression of inducible nitric oxide synthase, tumor necrosis factor α, CD16, CD32, and CD86 and increased the expression of the anti-inflammatory markers ARG1 and YM1. Taken together, our findings indicate that the cyclic guanosine monophosphate adenosine monophosphate synthase-stimulator of interferon genes-interferon regulatory factor 7 pathway plays a crucial role in the pathogenesis of Parkinson's disease.Copyright © 2025 Copyright: © 2025 Neural Regeneration Research.