Platelet-rich plasma in umbilical cord blood reduces neuropathic pain in spinal cord injury by altering the expression of ATP receptors.
Physiol Behav
; 228: 113186, 2021 01 01.
Article
em En
| MEDLINE
| ID: mdl-32980385
ABSTRACT
BACKGROUND:
Neuropathic pain following injury or dysfunction of the peripheral or CNS is one of the most important medical challenges to treat. Humane platelet-rich plasma (HPRP), which is a rich source of growth factors, may be able to treat and reduce pain caused by spinal cord injury (SCI). In this study, the effect of HPRP on neuropathic pain caused by SCI was investigated.METHODS:
Sixty adult male Wistar rats were randomly divided into 6 groups control, sham, SCI, vehicle (SCI+platelet-poor plasma), SCI+ PRP2day (injection 48 hrs after SCI) and SCI+PRP14day (injection 14 days after SCI). SCI was induced at the T12-T13 level. Behavioral tests were conducted weekly after injury for six weeks. Allodynia and hyperalgesia were assessed using acetone drops, plantar test and von Frey filament. Cavity size and the number of fibroblasts were determined by H&E stain, and the expression of mTOR, p-mTOR, P2×3R and P2Y4R were determined using the western blot technique. Data were analyzed using PRISM & SPSS software.RESULTS:
PRP injection showed a higher pain threshold in mechanical allodynia (p<0.0001), cold allodynia (p<0.0001) and thermal hyperalgesia (p<0.0001) than those in the spinal. Animals treated with PRP also reduced cavity size, fibroblast number, p-mTOR/mTOR ratio, and P2×3R expression, and increased P2Y4R expression. The difference between the two groups was not statistically significant.CONCLUSIONS:
The results showed that PRP reduced SCI-induced allodynia and hyperalgesia by regulating ATP signaling. Using HPRP can open a new window in the treatment of pain caused by damage to the nervous system.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Traumatismos da Medula Espinal
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Receptores Purinérgicos P2
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Plasma Rico em Plaquetas
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Neuralgia
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article