Fig. 8.

Schematic diagram showing the implantation of laser fibers in rats after SCI. Resting microglia and astrocytes begin to activate and participate in neuroinflammation after SCI. The activation of neurotoxic astrocytes is induced by the secretion of C1q, TNF-α, and IL-1α from activated microglia, and both neurotoxic microglia and neurotoxic astrocytes are harmful to neurons. The crosstalk of Lcn2/JAK2-STAT3 participates in the activation of microglia and astrocytes. Specifically, the JAK2-STAT3 pathway contributes to the activation of neurotoxic glial cells and the expression of Lcn2. In turn, Lcn2 exacerbates the activation of microglia and astrocytes and upregulates the activation of the JAK2-STAT3 pathway. The neuroprotective mechanism of PBM may be related to inhibition of the interaction of Lcn2 and the JAK2-STAT3 pathway, which is associated with neurotoxic microglia/astrocyte activation