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Ginsenoside Rg3 Suppresses Palmitate-Induced Apoptosis in MIN6N8 Pancreatic β-Cells

Chronic exposure to elevated levels of free fatty acids (FFA) causes β-cell dysfunction and may induce β-cell apoptosis in type 2 diabetes. The execution of β-cell apoptosis occurs through activation of mitogen-activated protein kinases (MAPKs). Ginsenoside Rg3 (Rg3), one of the active ingredients o...

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Detalles Bibliográficos
Autores principales: Kim, Kyong, Park, Min, Young Kim, Hye
Formato: Texto
Lenguaje:English
Publicado: the Society for Free Radical Research Japan 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803130/
https://www.ncbi.nlm.nih.gov/pubmed/20104262
http://dx.doi.org/10.3164/jcbn.09-49
Descripción
Sumario:Chronic exposure to elevated levels of free fatty acids (FFA) causes β-cell dysfunction and may induce β-cell apoptosis in type 2 diabetes. The execution of β-cell apoptosis occurs through activation of mitogen-activated protein kinases (MAPKs). Ginsenoside Rg3 (Rg3), one of the active ingredients of ginseng saponins, has not been known about the effects on β-cell apoptosis mediated with FFA. The aims of this study were to investigate the in vitro protective effects of Rg3 on MIN6N8 mouse insulinoma β-cells against FFA-induced apoptosis, as well as the modulating effects on p44/42 MAPK activation. Our results showed that Rg3 inhibited the palmitate-induced apoptosis through modulating p44/42 MAPK activation. We conclude that Rg3 has the potential role in suppressing the progression of type 2 diabetes by inhibiting FFA-mediated loss of β-cells.