To study the effect of photobiomodulation (PBM) on axon regeneration and secretion change of dorsal root ganglion (DRG) under oxidative stress after spinal cord injury (SCI), and further explore the effect of changes in DRG secretion caused by PBM on the polarization of macrophages. The PBM-DRG model was constructed to perform PBM on neurons under oxidative stress simulated in vitro. And the irradiation conditions were as follows: wavelength, 810 nm; power density, 2 mW/cm²; irradiation area, 4.5 cm²; and irradiation time, 440 s. Then resulted in an energy of 4 J (2 mW/cm² × 4.5 cm² × 440 s). About 100 μM H₂0₂ was added to the culture medium to simulate oxidative stress after SCI. An ROS (reactive oxygen species) assay kit was used to measure ROS contend in the DRG. The survival level of the neurons was measured using the CCK-8 method, and the axon regeneration of neurons was observed by using immunofluorescence. The secretion level of CCL2 from DRG was determined by RT-qPCR and ELISA. Further culturing macrophages of DRG-conditioned medium culture, the expression level of iNOS and Arg-1 in macrophages was assessed using Western blot analysis. The expression level of TNF-α and IL-1β was determined by ELISA. After adding the neutralizing antibody of CCL2 to the DRG neuron-conditioned medium following PBM irradiation to culture macrophages to observe the effects on macrophage polarization and secretion. PBM could reduce ROS levels in neurons, increase neuronal survival under oxidative stress, and promote neuronal axon regeneration. In addition, PBM could also promote CCL2 secretion by DRG under oxidative stress. By constructing a DRG supernatant-M1 macrophage adoptive culture model, we found that the supernatant of DRG after PBM intervention could reduce the expression level of iNOS and the secretion of TNF-α and IL-1β in M1 macrophages; at the same time, it could also up-regulate the expression of Arg-1, one of the markers of M2 macrophages. Furthermore, these effects could be prevented by the addition of neutralizing antibodies of CCL2. PBM could promote survival and axonal regeneration of DRG under SCI oxidative stress, increase the secretion level of CCL2 by DRG, and this change can reduce the polarization of macrophages to M1, further indicating that PBM could promote spinal cord injury repair.

研究光生物调节（PBM）对脊髓损伤（SCI）后氧化应激下背根神经节（DRG）轴突再生及分泌变化的影响，进一步探讨PBM引起的背根神经节分泌变化对神经元极化的影响。巨噬细胞。构建PBM-DRG模型以在体外模拟的氧化应激下对神经元进行PBM。并且照射条件如下：波长，810nm；功率密度，2 mW/cm ²；照射面积，4.5 cm ²；和辐照时间，440 s。然后产生 4 J (2 mW/cm ²  × 4.5 cm ²  × 440 s)的能量。约 100 μM H ₂ 0 ₂添加到培养基中以模拟 SCI 后的氧化应激。ROS（活性氧）检测试剂盒用于测量 DRG 中的 ROS 竞争。采用CCK-8法测定神经元存活水平，采用免疫荧光法观察神经元轴突再生情况。通过 RT-qPCR 和 ELISA 测定 DRG 中 CCL2 的分泌水平。进一步培养 DRG 条件培养基的巨噬细胞，使用蛋白质印迹分析评估巨噬细胞中 iNOS 和 Arg-1 的表达水平。通过ELISA测定TNF-α和IL-1β的表达水平。在PBM照射后将CCL2的中和抗体加入DRG神经元条件培养基培养巨噬细胞后，观察对巨噬细胞极化和分泌的影响。PBM 可以降低神经元中的 ROS 水平，增加氧化应激下的神经元存活率，并促进神经元轴突再生。此外，PBM 还可以促进 DRG 在氧化应激下分泌 CCL2。通过构建DRG上清液-M1巨噬细胞过继培养模型，我们发现PBM干预后DRG上清液可降低M1巨噬细胞中iNOS的表达水平和TNF-α和IL-1β的分泌；同时，它还可以上调M2巨噬细胞标志物之一Arg-1的表达。此外，可以通过添加 CCL2 的中和抗体来防止这些影响。PBM可以促进SCI氧化应激下DRG的存活和轴突再生，增加DRG分泌CCL2的水平，这种变化可以减少巨噬细胞向M1的极化，