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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...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
the Society for Free Radical Research Japan
2010
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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 |
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. |
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