Neuroprotective effects of violacein in a model of inherited amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive death of motor neurons and muscle atrophy, with defective neuron-glia interplay and emergence of aberrant glial phenotypes having a role in disease pathology. Here, we have studied if the pigment violacei...

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Detalles Bibliográficos
Autores: Olivera Bravo, Silvia, Bolatto Pereira, Carmen Isabel Selene, Otero Damianovich, Nicolás Gabriel, Stancov Iturrioz, Matías, Cerri Fassio, Sofía Natalia, Rodríguez, Paola, Boragno, Daniela, Cuitiño, María Noel, Larrambembere, Fernanda, Isasi, Eugenia, Marco, Marta, Alem, Diego, Canclini, Lucía, Hernandéz Mir, karina, Davyt, Danilo
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2022
País:Uruguay
Institución:Universidad de la República
Repositorio:COLIBRI
Idioma:inglés
OAI Identifier:oai:colibri.udelar.edu.uy:20.500.12008/39131
Acceso en línea:https://hdl.handle.net/20.500.12008/39131
Access Level:acceso abierto
Palabra clave:Cell biology
Neuroscience
Descripción
Sumario:Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive death of motor neurons and muscle atrophy, with defective neuron-glia interplay and emergence of aberrant glial phenotypes having a role in disease pathology. Here, we have studied if the pigment violacein with several reported protective/antiproliferative properties may control highly neurotoxic astrocytes (AbAs) obtained from spinal cord cultures of symptomatic hSOD1G93A rats, and if it could be neuroprotective in this ALS experimental model. At concentrations lower than those reported as protective, violacein selectively killed aberrant astrocytes. Treatment of hSOD1G93A rats with doses equivalent to the concentrations that killed AbAs caused a marginally significant delay in survival, partially preserved the body weight and soleus muscle mass and improved the integrity of the neuromuscular junction. Reduced motor neuron death and glial reactivity was also found and likely related to decreased inflammation and matrix metalloproteinase-2 and -9. Thus, in spite that new experimental designs aimed at extending the lifespan of hSOD1G93A rats are needed, improvements observed upon violacein treatment suggest a significant therapeutic potential that deserves further studies.

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