Effects of local and systemic treatment with human natural killer-1 mimetic peptide (HNK-1) after ventral root avulsion and reimplantation in mice
J. venom. anim. toxins incl. trop. dis
;
30: e20230065, 2024. tab, graf
Artigo
em Inglês
|
LILACS-Express
| LILACS, VETINDEX
| ID: biblio-1558351
ABSTRACT
Abstract Background:
Spinal ventral root injuries generate significant motoneuron degeneration, which hinders full functional recovery. The poor prognosis of functional recovery can be attributed to the use or combination of different therapeutic approaches. Several molecules have been screened as potential treatments in combination with surgical reimplantation of the avulsed roots, the gold standard approach for such injuries. Among the studied molecules, human natural killer-1 (HNK-1) stands out as it is related to the stimulation of motor axon outgrowth. Therefore, we aimed to comparatively investigate the effects of local administration of an HNK-1 mimetic peptide (mp-HNK-1) and systemic treatment with ursolic acid (UA), another HNK-1 mimetic, after ventral root avulsion and reimplantation with heterologous fibrin biopolymer (HFB).Methods:
Female mice of the isogenic strain C57BL/6JUnib were divided into five experimental groups Avulsion, Reimplantation, mp-HNK-1 (in situ), and UA (systemic treatment). Mice were evaluated 2 and 12 weeks after surgery. Functional assessment was performed every four days using the Catwalk platform. Neuronal survival was analyzed by cytochemistry, and glial reactions and synaptic coverage were evaluated by immunofluorescence.Results:
Treatment with UA elicited long-term neuroprotection, accompanied by a decrease in microglial reactions, and reactive astrogliosis. The neuroprotective effects of UA were preceded by increased glutamatergic and GABAergic inputs in the ventral spinal cord two weeks after injury. However, a single application of mp-HNK-1 had no significant effects. Functional analysis showed that UA treatment led to an improvement in motor and sensory recovery.Conclusion:
Overall, the results indicate that UA is neuroprotective, acting on glial cells and synaptic maintenance, and the combination of these findings led to a better functional recovery.
Texto completo:
DisponíveL
Índice:
LILACS (Américas)
Idioma:
Inglês
Revista:
J. venom. anim. toxins incl. trop. dis
Assunto da revista:
Toxicologia
Ano de publicação:
2024
Tipo de documento:
Artigo
/
Documento de projeto
País de afiliação:
Brasil
/
Alemanha
Instituição/País de afiliação:
São Paulo State University/BR
/
University of Campinas/BR
/
University of Saarland/DE
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