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

Ni Komang Sri Dewi Untari,Guritno Suryokusumo,Kurnia Kusumastuti,I Ketut Sudiana,Moacyr Rego

doi:10.1155/2021/6627779

Ni Komang Sri Dewi Untari, Guritno Suryokusumo + Show 3 more

Open Access

https://doi.org/10.1155/2021/6627779

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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.

Highlights

Guillain–Barre Syndrome (GBS) represents the most common disease, which results in acute flaccid paralysis
Histopathological features divide GBS into demyelinating and axonal subtypes, which are called acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). e existing evidence suggests that peripheral nerve-binding autoantibodies followed by complement deposition may result in neuronal damage in both AIDP and AMAN [1]
AMAN constitutes a form of GBS, which is commonly found in China, Japan, and Central and South America with a frequency of around 35–65%

Summary

Introduction

Guillain–Barre Syndrome (GBS) represents the most common disease, which results in acute flaccid paralysis. Histopathological features divide GBS into demyelinating and axonal subtypes, which are called acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). E existing evidence suggests that peripheral nerve-binding autoantibodies followed by complement deposition may result in neuronal damage in both AIDP and AMAN [1]. Patients with AMAN are associated with motor neuron damage in the nodes of Ranvier [2]. AMAN is generally associated with Campylobacter jejuni (C. jejuni) and Zika virus infection [3]. Disability is often found in patients treated with standard therapy for months [4]. Autoimmune Diseases conventional therapy is unsatisfactory due to its high cost and some complications

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