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Protective effects of extracellular polymeric substances from Aphanizomenon flos-aquae on neurotoxicity induced by local anesthetics

The neurotoxicity of local anesthetics has received an increasing amount of attention and more effective therapeutic agents are required. Extracellular polymeric substances from Aphanizomenon flos-aquae (EPS-A) are high molecular weight polysaccharides. The present study aimed to elucidate the prote...

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Detalles Bibliográficos
Autores principales: Xue, Xing, Lv, Ying, Leng, Yufang, Zhang, Yan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6125984/
https://www.ncbi.nlm.nih.gov/pubmed/30214519
http://dx.doi.org/10.3892/etm.2018.6540
Descripción
Sumario:The neurotoxicity of local anesthetics has received an increasing amount of attention and more effective therapeutic agents are required. Extracellular polymeric substances from Aphanizomenon flos-aquae (EPS-A) are high molecular weight polysaccharides. The present study aimed to elucidate the protective effects of EPS-A on neurotoxicity induced by local anesthetics in an intraperitoneal injection bupivacaine rat model. The results of immunohistochemical staining inicated that following intraperitoneal injection of EPS-A the levels of apoptosis and caspase-3 decreased, and the expression levels of microtubule-associated protein 1A light chain 3 (LC3) and beclin1 increased. In order to further clarify the mechanism of the EPS-A-mediated protection, the expression of key proteins associated with autophagy was investigated by western blotting. The results suggested that the ratio of LC3-II/LC3-I and the expression level of beclin1 increased. Taken together, the results indicated that EPS-A induced neuroprotective effects on bupivacaine-induced neurotoxicity. The underlying mechanism may be associated with the inhibition of apoptosis, upregulation of autophagy and improvement of cell survival. The results suggested that EPS-A may be a candidate neuroprotective agent against neurotoxicity caused by local anesthetics.