Role of calmodulin-dependent protein kinase II in bupivacaine hydrochloride-induced injury of SH-SY5Y cells / 南方医科大学学报
Journal of Southern Medical University
;
(12): 1133-1136, 2015.
Artigo
em Chinês
| WPRIM
| ID: wpr-333669
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of KN93, a calmodulin-dependent protein kinase II (CaMK II) inhibitor, on SH-SY5Y cell injury induced by bupivacaine hydrochloride.</p><p><b>METHODS</b>SH-SY5Y cells exposed for 24 h to 1 mmol/L KN93, 1 mmol/L bupivacaine hydrochloride, or both were examined for morphological changes and Cav3.1 protein expressions using Western blotting. The vitality and apoptosis rate of the cells at different time points during the exposures were assessed with MTT assay and flow cytometry, respectively.</p><p><b>RESULTS</b>Bupivacaine hydrochloride exposure caused obvious cell morphologial changes, reduced cell viability, increased cell apoptosis, and enhanced Cav3.1 protein expression. All these changes were partly reversed by treatment of the cells with 1 mmol/L KN93.</p><p><b>CONCLUSIONS</b>CaMKII may play a role in bupivacaine hydrochloride-induced SH-SY5Y cells injury, which is related with upregulated Cav3.1 protein expression.</p>
Texto completo:
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Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Bupivacaína
/
Regulação para Cima
/
Linhagem Celular
/
Sobrevivência Celular
/
Apoptose
/
Canais de Cálcio Tipo T
/
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina
/
Metabolismo
Limite:
Humanos
Idioma:
Chinês
Revista:
Journal of Southern Medical University
Ano de publicação:
2015
Tipo de documento:
Artigo
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