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Korean Red Ginseng inhibits apoptosis in neuroblastoma cells via estrogen receptor b-mediated phosphatidylinositol-3 kinase/Akt signaling

Background: Ginseng has been shown to exert antistress effects both in vitro and in vivo. However, theeffects of ginseng on stress in brain cells are not well understood. This study investigated how KoreanRed Ginseng (KRG) controls hydrogen peroxide-induced apoptosis via regulation of phosphatidylin...

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Published in:Journal of ginseng research 2015, 39(1), , pp.69-75
Main Authors: Cuong Thach Nguyen, Truc Thanh Luong, 김규리, 표석능, 이동권
Format: Article
Language:English
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Summary:Background: Ginseng has been shown to exert antistress effects both in vitro and in vivo. However, theeffects of ginseng on stress in brain cells are not well understood. This study investigated how KoreanRed Ginseng (KRG) controls hydrogen peroxide-induced apoptosis via regulation of phosphatidylinositol-3 kinase (PI3K)/Akt and estrogen receptor (ER)-b signaling. Methods: Human neuroblastoma SK-N-SH cells were pretreated with KRG and subsequently exposed toH2O2. The ability of KRG to inhibit oxidative stress-induced apoptosis was assessed in MTT cytotoxicityassays. Apoptotic protein expression was examined byWestern blot analysis. The roles of ER-b, PI3K, andp-Akt signaling in KRG regulation of apoptosis were studied using small interfering RNAs and/or targetantagonists. Results: Pretreating SK-N-SH cells with KRG decreased expression of the proapoptotic proteins p-p53and caspase-3, but increased expression of the antiapoptotic protein BCL2. KRG pretreatment was alsoassociated with increased ER-b, PI3K, and p-Akt expression. Conversely, ER-b inhibition with smallinterfering RNA or inhibitor treatment increased p-p53 and caspase-3 levels, but decreased BCL2, PI3K,and p-Akt expression. Moreover, inhibition of PI3K/Akt signaling diminished p-p53 and caspase-3 levels,but increased BCL2 expression. Conclusion: Collectively, the data indicate that KRG represses oxidative stress-induced apoptosis byenhancing PI3K/Akt signaling via upregulation of ER-b expression. KCI Citation Count: 48
ISSN:1226-8453
2093-4947