Background: Adalimumab, a new-generation anti-inflammatory agent, exerts its effect through tumor necrosis factor α (TNF-α), secreted from immune response cells such as macrophages and lymphocytes. TNF-α has been shown to play an important role in the processes of apoptosis and demyelination, and blockage of its activity may improve neural healing. Investigated in the present study is the probable neuroprotective influence of adalimumab in rats using a peripheral nerve injury model with biochemical and electron microscopic methods.
Methods: Forty adult Wistar albino rats were randomly divided into control, sciatic nerve trauma, low-dose adalimumab, and high-dose adalimumab groups. Six rats from each group were assigned biochemical microscopy, and 4 were assigned electron microscopy. Neural injury was induced with clip compression following dissection of sciatic nerves. Adalimumab was simultaneously injected. The rats were sacrificed after 2 weeks of adalimumab treatment.
Results: Nerve tissue lipid peroxidation values were found to be significantly decreased in both the low- and high-dose adalimumab treatment groups, compared to the group subjected only to sciatic nerve trauma.
Conclusion: Results demonstrate that adalimumab is an effective neuroprotective agent for neural healing, particularly in the early phase.