| Objective: To investigate the effects of chondroitinase ABC (ChABC) on axonalmyelination and glial scar after spinal cord injury (SCI) in rats.Methods: Seventy-two adult male Sprague Dawley rats were randomly assigned intoChABC treatment group (group A), saline treatment group (group B), and sham operationgroup (group C),24rats in each group. In groups A and B, the SCI model was establishedwith modified Allen’s method and then the rats of groups A and B were administrated bysubarachnoid injection of6μL ChABC (1U/mL) and saline respectively at1hour afterinjury and every day for1week; the rats of group C served as control, which canal wasopened without damage to spinal cord.At1,7,14, and28days after operation, thelocomotor functions were evaluated according to the Basso-Beattie-Bresna-han (BBB)score scale; and the spinal cord samples were harvested for HE staining, Nissl staining,andimmunohistochemistry analysis to detect the change of myel in basic protein (MBP),growth associated protein43(GAP-43), and glial fibrillary acidic protein (GFAP) of theinjured spinal cord.Results: At different time points, the BBB score of group C was significantly higherthan those of groups A and B (P <0.05),and the BBB score of group A was significantlybetter than that of group B at14and28days after operation (P <0.05). HE staining andNissl staining showed that the morphous and the neuron number of the remainant injuredspinal cord in group A were better than those in group B. The integral optical density (IOD)values of MBP and GAP-43and the positive area of GFAP after SCI in groups A and Bwere significantly higher than those in group C at different time points (P <0.05), and IODvalues of MBP and GAP-43were significantly higher in group A than those in group B at7,14, and28days after operation (P <0.05), but the positive area of GFAP was significantlysmaller in group A than that in group B (P <0.05).Conclusions: The ChABC can effectively improve the microenvironment of theinjured spinal cord of rats, enhance the expressions of MBP and GAP-43, and inhibit the expression of GFAP, which promotes the axonal regeneration and myelination, attenuateglial scar formation, and promote the recovery of nerve function. |
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