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Ginsenoside Rg3 Suppresses Palmitate-Induced Apoptosis in MIN6N8 Pancreatic beta-Cells.

Kim K, Park M, Young Kim H - J Clin Biochem Nutr (2009)

Bottom Line: Ginsenoside Rg3 (Rg3), one of the active ingredients of ginseng saponins, has not been known about the effects on beta-cell apoptosis mediated with FFA.The aims of this study were to investigate the in vitro protective effects of Rg3 on MIN6N8 mouse insulinoma beta-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.

View Article: PubMed Central - PubMed

Affiliation: Functional Food Technology Research Group, Research Division for Emerging Innovative Techology, Korea Food Research Institute, 516 Baekhyun-dong, Bundang-gu, Songnam-si, Kyonggi-do 463-746, Republic of Korea.

ABSTRACT
Chronic exposure to elevated levels of free fatty acids (FFA) causes beta-cell dysfunction and may induce beta-cell apoptosis in type 2 diabetes. The execution of beta-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 beta-cell apoptosis mediated with FFA. The aims of this study were to investigate the in vitro protective effects of Rg3 on MIN6N8 mouse insulinoma beta-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 beta-cells.

No MeSH data available.


Related in: MedlinePlus

Effect of ginsenoside Rg3 on palmitate-induced activation of p44/42 MAPK in MIN6N8 cells. (A) Time course of p44/42 activation with palmitate exposure to MIN6N8 cells. The cells were administrated with 500 µM palmitate for the indicated time points and harvested for whole-cell lysates to be used in Western blots. Total p44/42 was probed as well. All data are representative of three independent experiments. (B) Effect of Rg3 on palmitate-induced phosphorylation of p44/42 in the cells. The cells were treated with palmitate in the presence or absence of Rg3 for 48 h, and Western blot analysis was performed. All data are representative of three independent experiments.
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Figure 3: Effect of ginsenoside Rg3 on palmitate-induced activation of p44/42 MAPK in MIN6N8 cells. (A) Time course of p44/42 activation with palmitate exposure to MIN6N8 cells. The cells were administrated with 500 µM palmitate for the indicated time points and harvested for whole-cell lysates to be used in Western blots. Total p44/42 was probed as well. All data are representative of three independent experiments. (B) Effect of Rg3 on palmitate-induced phosphorylation of p44/42 in the cells. The cells were treated with palmitate in the presence or absence of Rg3 for 48 h, and Western blot analysis was performed. All data are representative of three independent experiments.

Mentions: When MIN6N8 cells were incubated with 500 µM palmitate and analyzed over a 48-h, p44/42 MAPK activation, as evidenced by phosphorylation of what appeared to be two isoforms, was noted at 48 h after administration with palmitate (Fig. 3A). To explore the involvement of p44/42 MAPK in the mechanism of protection by Rg3, we examined the effects of Rg3 on palmitate-mediated p44/42 MAPK activation. Based on the results of Western blot, it was found that co-treatment of the cells with Rg3 (0.1–5.0 µM) suppressed palmitate-induced phosphorylation of p44/42 MAPK (Fig. 3B).


Ginsenoside Rg3 Suppresses Palmitate-Induced Apoptosis in MIN6N8 Pancreatic beta-Cells.

Kim K, Park M, Young Kim H - J Clin Biochem Nutr (2009)

Effect of ginsenoside Rg3 on palmitate-induced activation of p44/42 MAPK in MIN6N8 cells. (A) Time course of p44/42 activation with palmitate exposure to MIN6N8 cells. The cells were administrated with 500 µM palmitate for the indicated time points and harvested for whole-cell lysates to be used in Western blots. Total p44/42 was probed as well. All data are representative of three independent experiments. (B) Effect of Rg3 on palmitate-induced phosphorylation of p44/42 in the cells. The cells were treated with palmitate in the presence or absence of Rg3 for 48 h, and Western blot analysis was performed. All data are representative of three independent experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2803130&req=5

Figure 3: Effect of ginsenoside Rg3 on palmitate-induced activation of p44/42 MAPK in MIN6N8 cells. (A) Time course of p44/42 activation with palmitate exposure to MIN6N8 cells. The cells were administrated with 500 µM palmitate for the indicated time points and harvested for whole-cell lysates to be used in Western blots. Total p44/42 was probed as well. All data are representative of three independent experiments. (B) Effect of Rg3 on palmitate-induced phosphorylation of p44/42 in the cells. The cells were treated with palmitate in the presence or absence of Rg3 for 48 h, and Western blot analysis was performed. All data are representative of three independent experiments.
Mentions: When MIN6N8 cells were incubated with 500 µM palmitate and analyzed over a 48-h, p44/42 MAPK activation, as evidenced by phosphorylation of what appeared to be two isoforms, was noted at 48 h after administration with palmitate (Fig. 3A). To explore the involvement of p44/42 MAPK in the mechanism of protection by Rg3, we examined the effects of Rg3 on palmitate-mediated p44/42 MAPK activation. Based on the results of Western blot, it was found that co-treatment of the cells with Rg3 (0.1–5.0 µM) suppressed palmitate-induced phosphorylation of p44/42 MAPK (Fig. 3B).

Bottom Line: Ginsenoside Rg3 (Rg3), one of the active ingredients of ginseng saponins, has not been known about the effects on beta-cell apoptosis mediated with FFA.The aims of this study were to investigate the in vitro protective effects of Rg3 on MIN6N8 mouse insulinoma beta-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.

View Article: PubMed Central - PubMed

Affiliation: Functional Food Technology Research Group, Research Division for Emerging Innovative Techology, Korea Food Research Institute, 516 Baekhyun-dong, Bundang-gu, Songnam-si, Kyonggi-do 463-746, Republic of Korea.

ABSTRACT
Chronic exposure to elevated levels of free fatty acids (FFA) causes beta-cell dysfunction and may induce beta-cell apoptosis in type 2 diabetes. The execution of beta-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 beta-cell apoptosis mediated with FFA. The aims of this study were to investigate the in vitro protective effects of Rg3 on MIN6N8 mouse insulinoma beta-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 beta-cells.

No MeSH data available.


Related in: MedlinePlus