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. 2023 Jul 10;16:1214294. doi: 10.3389/fnmol.2023.1214294

Figure 1.

Figure 1

Simplified schematic representation- underlying mechanisms of IL-10 in the treatment of SCI. Binding to its receptor, IL-10 phosphorylates JAK1 and Tyk2, which activate cascaded signaling of STAT3 and PI3K/Akt/mTOR pathways. In the IL-10/STAT3 axis, the expression of SOCS3 exerts an obvious immune-inflammatory regulation and efficiently inhibits P38 MAPK pathway. This leads to a decrease of IL-1β, IL-6, TNFα, caspase 3, iNOS, which ultimately limits the secondary injury. Additionally, STAT3 activation drives the expression of β-endorphin, resulting in an antinociceptive effect. The expression of Ddit4 suppresses the activity of mTORC1 and promotes dysfunctional mitophagy, which plays an important role in the anti-oxidative stress effect. The IL-10/PI3K/Akt/mTOR pathway promotes cell survival, migration by regulating the transcription of ULK1, S6K1, BAD, MDM2 which improve the expression of anti-apoptotic protein (Bcl-xl, Bcl-2), and the surface adhesion molecules/chemokine receptors, MMP, CCR5. These events facilitate the migration of adult neural stem cells. Through these mechanisms, IL-10 demonstrates multi-neuroprotective effects in SCI. The pathway was drawn by Pathway Builder Tool 2.0.