Protective Effect of Hyperbaric Oxygen Treatment on Axon Degeneration after Acute Motor Axonal Neuropathy

Abstract

Objectives. Acute motor axonal neuropathy (AMAN) is a disease that leads to acute flaccid paralysis and may result from the binding of antibody and antigen to the spinal cord. The objective of this study is to evaluate the protective effect of hyperbaric oxygen treatment (HBOT) on axon degeneration of the spinal cord and sciatic nerve of the AMAN model rabbit. Axonal degeneration was assessed by evaluating glutathione (GSH) activity, interleukin-1β (IL-1β) expression, and clinical and histopathological features. Methods. Twenty-one New Zealand rabbits were divided into three groups. The treatment group was exposed to 100% oxygen at 2.4 ATA 90 minutes for 10 days at a decompression rate of 2.9 pounds per square inch/minute. GSH level was evaluated using an enzyme-linked immune-sorbent assay. An expression of IL-1β in the spinal cord was determined by immunohistochemistry. Clinical appearances were done by motor scale and body weight. Histological features observed neuronal swelling and inflammatory infiltration in the sagittal lumbar region and the undulation of the longitudinal sciatic nerve. Results. Rabbits exposed to HBO had high GSH activity levels ( $p<0.05$ ) but unexpectedly had high IL1β expression ( $p>0.05$ ). In addition, the HBO-exposed rabbits had a better degree of undulation, the size of neuronal swelling was smaller, the number of macrophages was higher, and motor function was better than the AMAN model rabbits ( $p<0.05$ ). Conclusions. These findings indicate that HBO therapy can decrease axon degeneration by triggering GSH activity, increasing IL-1β level, and restoring tissues and motor status. In conclusion, HBO has a protective effect on axon degeneration of the spinal cord and sciatic nerve of the AMAN model rabbit.