Curcumin-activated olfactory ensheathing cells attenuate astroglial scar to facilitate nerve repair via the IL-10/NF-κB axis after spinal cord injury.

Excessive astrocyte activation following spinal cord injury (SCI) can trigger the substantial deposition of inhibitory extracellular matrix components, particularly chondroitin sulfate proteoglycans (CSPGs) at the lesion core. This astroglial response typically leads to the formation of dense glial scars, which profoundly impede neuronal regeneration and axonal extension. In this study, we show that transplantation of curcumin-activated olfactory ensheathing cells (aOECs) markedly promotes nervous tissue reorganization in SCI rats, as evidenced by reduced lesion cavitation and aligned GFAP-positive cells along the lesion border. Concurrently, aOECs effectively downregulate the expression of glial fibrillary acidic protein (GFAP) and Vimentin, reduce CSPGs deposition, and upregulate neuronal markers β-Tubulin (Tuj-1) and Neurofilament-light chain (NF-68), highlighting a dual role in suppressing glial scar formation and promoting neural regeneration. Notably, these beneficial effects are reversed by IL-10 knockdown. Mechanistically, aOECs significantly upregulate IL-10 secretion, thereby suppressing the activation of the nuclear factor kappa B (NF-κB) signaling pathway, as evidenced by decreased phosphorylated IκB (p-IκB) and NF-κB subunit p65 proteins, along with reduced complement 3 (C3) expression. In summary, our findings demonstrate that IL-10 mediates aOECs-induced suppression of astroglial scar formation in SCI rats, thereby promoting neuronal survival, axonal preservation, and motor function recovery. The underlying mechanism likely involves regulation of astrocyte phenotypic switch via the IL-10/NF-κB signaling axis. These results provide experimental support for the potential clinical translation of aOEC-based therapies in SCI.