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Animal study demonstrates that paclitaxel-loaded fibrin scaffolds after subacute scar resection improve functional recovery in rats, indicating potential for spinal cord repair.
Scar tissue impede axonal regeneration and hinder functional recovery after spinal cord injury. Previous studies have demonstrated excision of scar tissue during the subacute phase (particularly on day 10) not only enhances neuronal regeneration but also identifies microtubule stabilization as a key contributor to axonal regeneration in this process. Here we grafted fibrin scaffolds loaded with paclitaxel (a microtubule-stabilizing agent) immediately after scar excision during subacute stage, with the aim of stabilizing axonal microtubules. Our results showed that paclitaxel promoted functional recovery of injured rats by enhancing neuronal regeneration and axonal elongation post resecting scars in subacute stage. In paclitaxel-fibrin-grafted group, the microenvironment post injury was significantly improved. The secretion of pro-regenerative factors (laminin, BDNF and NT-3) was upregulated and the deposition of CSPG, a key inhibitory component of the scar tissue, was reduced in injured spinal tissue under paclitaxel-fibrin. Moreover, BSCB (blood spinal cord barrier) was reconstructed that alleviated the continuous infiltration of immune cells into the lesion site. Collectively, these findings suggest that the administration of paclitaxel following scar resection during subacute stage may hold significant potential in the treatment of SCI.
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Liu et al. (2026) studied this question.
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