Edaravone Improves Motor Dysfunction Following Brachial Plexus Avulsion Injury in Rats.

Brachial plexus root avulsion (BPRA) is often caused by road collisions, leading to total loss of motor function in the upper limb. At present, effective treatment options remain limited. Edaravone (EDA), a substance that eliminates free radicals, exhibits numerous biological properties, including neuroprotective, antioxidant and anti-inflammatory effects. However, the specific role and molecular mechanisms of EDA in the treatment of BPRA remain to be fully elucidated. The present study used a rat model of BPRA, following avulsion of the fifth, sixth and seventh cervical (C5, C6 and C7) anterior roots. Notably, C6 was replanted following a subcutaneous injection of either saline or 30 mg/kg/day EDA for seven continuous days. Subsequently, behavioral, histochemical, Western blot and reverse transcription-quantitative PCR (RT-PCR) analyses were conducted. Results of the present study revealed that treatment with EDA improves motor dysfunction, indicated by the increased Grooming test score, usage of the affected limb, and Irvine, Beatties and Bresnahan (IBB) score, following BPRA. In addition, EDA reduced the death of motoneurons (MNs), indicated by the increased number of Nissl-positive neuron, at the site of the affected limb, inhibited neuroinflammation and cellular pyroptosis, indicated by the decreased expression levels of IL-1β, IL-6, TNF-α, IL-18, p-p65, NLRP3, GSDMD and Caspase-1, improved the morphology of the abnormal myocutaneous nerve fibers, promoted axon remyelination, indicated by increased mRNA expression levels of remyelination-associated genes, including egr2, GAP-43, hmgcr, L1CAM, mpz, pmp22 and prx and demyelination-associated genes, including ngfr, notch1, pou3f1 and sox2, and alleviated muscle atrophy, indicated by the increased weight and volume of biceps brachii muscle, and the decreased number of fibroblasts and increased diameters in the fibers. Collectively, results of the present study suggested that EDA may support axonal remyelination and inhibit pyroptosis-associated neuroinflammation, enhancing MN survival and facilitating functional motor recovery. Thus, the present study may provide a novel theoretical basis for the use of EDA in the treatment of BPRA.