Neural Regeneration Research (Jan 2015)
Early cyclosporin A treatment retards axonal degeneration in an experimental peripheral nerve injection injury model
- Ibrahim Erkutlu,
- Mehmet Alptekin,
- Sirma Geyik,
- Abidin Murat Geyik,
- Inan Gezgin,
- Abdulvahap Gök
Affiliations
- Ibrahim Erkutlu
- Mehmet Alptekin
- Sirma Geyik
- Abidin Murat Geyik
- Inan Gezgin
- Abdulvahap Gök
- DOI
- https://doi.org/10.4103/1673-5374.152381
- Journal volume & issue
-
Vol. 10,
no. 2
pp. 266 – 270
Abstract
Injury to peripheral nerves during injections of therapeutic agents such as penicillin G potassium is common in developing countries. It has been shown that cyclosporin A, a powerful immunosuppressive agent, can retard Wallerian degeneration after peripheral nerve crush injury. However, few studies are reported on the effects of cyclosporin A on peripheral nerve drug injection injury. This study aimed to assess the time-dependent efficacy of cyclosporine-A as an immunosuppressant therapy in an experimental rat nerve injection injury model established by penicillin G potassium injection. The rats were randomly divided into three groups based on the length of time after nerve injury induced by penicillin G potassium administration (30 minutes, 8 or 24 hours). The compound muscle action potentials were recorded pre-injury, early post-injury (within 1 hour) and 4 weeks after injury and compared statistically. Tissue samples were taken from each animal for histological analysis. Compared to the control group, a significant improvement of the compound muscle action potential amplitude value was observed only when cyclosporine-A was administered within 30 minutes of the injection injury (P < 0.05); at 8 or 24 hours after cyclosporine-A administration, compound muscle action potential amplitude was not changed compared with the control group. Thus, early immunosuppressant drug therapy may be a good alternative neuroprotective therapy option in experimental nerve injection injury induced by penicillin G potassium injection.
Keywords
- Alzheimer′s disease
- amyloid-β
- astrocytes
- Ca 2+
- calcilytic
- calcium-sensing receptor
- nitromemantine
- NPS 2143
- α7-nicotinic acetylcholine receptor
- nerve regeneration
- spinal cord injury
- surgical decompression
- tumor necrosis factor α
- cell apoptosis
- neurological function
- neural regeneration
- nerve regeneration
- spinal cord injury
- contusion
- Nogo-A
- axon growth
- immunohistochemistry
- fluorescent quantitative PCR
- neural regeneration
- nerve regeneration
- spinal cord injury
- Schwann cells
- cell transplantation
- edaravone
- motor function
- electrophysiological function
- neural regeneration
- nerve regeneration
- electroacupuncture
- intervertebral disc
- blood circulation
- inflammation
- neuroprotection
- motor function
- neurons
- NSFC grants
- neural regeneration
- nerve regeneration
- astrocytoma
- mice
- immunodeficiency (BALB/c) mice
- Notch
- nestin
- glial fibrillary acidic protein
- CD133
- spinal cord
- brain
- MRI
- neural regeneration
- nerve regeneration
- earthquake
- peripheral nerve injury
- LSUHSC score
- compartment syndrome
- surgery therapy
- physiotherapy
- nerve decompression
- neural regeneration
- nerve regeneration
- brachial plexus injury
- human amniotic epithelial cells
- forepaw function
- stress relaxation
- creep
- viscoelasticity
- neural regeneration
- nerve regeneration
- peripheral nerve injury
- injection injury
- cyclosporine A
- penicillin G potassium
- Wallerian degeneration
- neuroelectrophysiology
- neural regeneration