Ginsenoside F₂ induces apoptosis in humor gastric carcinoma cells through reactive oxygen species-mitochondria pathway and modulation of ASK-1/JNK signaling cascade in vitro and in vivo

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• 作者：Qian Mao^a ; ¹ ; Ping-Hu Zhang^b ; ¹ ; Qiang Wang^c ; ^{qwang49@126.com" class="auth_mail} ; Song-Lin Li^a ; ^{songlinli64@126.com" class="auth_mail}
• 关键词：Ginsenoside F2 ; Apoptosis ; ASK-1/JNK ; Mitochondria ; ROS ; Subcutaneous tumor model
• 刊名：Phytomedicine
• 出版年：15 March, 2014
• 年：2014
• 卷：21
• 期：4
• 页码：515-522
• 全文大小：2564 K

文摘

Ginsenoside F₂ (F₂) is a potential bioactive metabolite of major ginsenosides. The potential anti-cancer effect of F₂ in gastric cancer cells has not been appraised. This study investigated the effects of F₂ on the production of reactive oxygen species (ROS). We also investigated the in vitro and in vivo effects of F₂ on the downstream signaling pathways leading to apoptosis in human gastric cancer cells. The in vitro data revealed that F₂ induces ROS accumulation followed by a decrease in mitochondrial transmembrane potential (MTP), and the release of cytochrome c (cyto c), which induced the caspase-dependent apoptosis. Further assay indicated that modulation of ASK-1/JNK pathway contributes to apoptosis. In vivo, F₂ exhibits the obvious anti-cancer effect compared with cisplatin with no obvious toxicity. Jointly, these results suggest that F₂ induces apoptosis by causing an accumulation of ROS and activating the ASK-1/JNK signaling pathway. This provides further support for the use of F₂ as a novel anticancer therapeutic candidate.