Polysaccharides from Portulaca oleracea L. regulated insulin secretion in INS-1 cells through voltage-gated Na+ channel.
Biomed Pharmacother
; 109: 876-885, 2019 Jan.
Article
em En
| MEDLINE
| ID: mdl-30551541
ABSTRACT
The present study was undertaken to determine the involvement of voltage-gated Na+ channel (VGSC) and other mechanism related to insulin secretion in polysaccharides from Portulaca oleracea L. (POP)-induced secretion of insulin from insulin-secreting ß-cell line cells (INS-1) cells. Our results showed that the concentration of insulin both in culture medium and inside INS-1 cells were increased under the existing of different concentration of glucose by POP or TTX, respectively. However, the effect POP on insulin secretion and production were blocked by TTX, a VGSC blocker. Meanwhile, POP improved the mitochondrial membrane potential (Δψm), increased adenosine triphosphate (ATP) production, depolarized cell membrane potential (MP) and increased intracellular Ca2+ levels ([Ca2+]i). Furthermore, POP treatment increased the expression level of Nav1.3 and decreased the expression level of Nav1.7. TTX treatment decreased the expression level of Nav1.3 and Nav1.7. On the other hand, POP also elevated the survival of INS-1 cells. These results suggested that POP induced-secretion/production of insulin in INS-1 cells were mediated by VGSC through its change of function and subunits expression and subsequent VGSC- dependent events such as change of intracellular Ca2+ releasing, ATP metabolism, cell membrane and mitochondrial membrane potential, and also improvement of INS-1 cell survival. Meanwhile, our data indicated the potentiality of developing POP to be a drug for diabetes treatment and VGSC as a therapeutic target in diabetes treatment is valuable to be investigated further.
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Base de dados:
MEDLINE
Assunto principal:
Polissacarídeos
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Extratos Vegetais
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Portulaca
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Células Secretoras de Insulina
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Canais de Sódio Disparados por Voltagem
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Insulina
Idioma:
En
Revista:
Biomed Pharmacother
Ano de publicação:
2019
Tipo de documento:
Article