Role of ginsenosides in reactive oxygen species-mediated anticancer therapy
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Islam M.D. Sodrul1,2, Chenying Wang1, Xiangfeng Chen1, Jing Du1 and Hongxiang Sun1
1Key Laboratory of Animal Virology of Ministry of Agriculture, College of Animal Sciences, Zhejiang University, Hangzhou, China
2Departments of Physiology and Pharmacology, Bangabandhu Sheikh Mujibur Rahman Agricultural University, Gazipur, Bangladesh
Hongxiang Sun, email: email@example.com
Keywords: ginsenosides; ROS; cancer; anticancer therapy; mechanism
Received: August 14, 2017 Accepted: December 05, 2017 Published: December 19, 2017
Cancer is still a global public health problem, which is the leading cause of death in most countries. Ginseng has been used for centuries all over the world as a panacea that promotes longevity. As the king of herb plants, ginseng holds great promise as a new treatment option which is used either by itself or in combination with other medicinal ingredients that is widely accepted as complementary and alternative medicine in cancer therapy. Ginsenosides, the major pharmacologically active ingredients of ginseng, have been shown to have multiple medicinal effects including prominent anticancer activity. The purpose of this review is to give our perspective about the roles of ginsenosides in reactive oxygen species (ROS)-mediated anticancer therapy. Additionally, to provide new sheds light for further improvement and carry out pre-clinical and clinical trials to develop it successfully into a potential anticancer agent. Panax herbs and their derivate/metabolites ginsenosides exert beneficial effects for treating various types of cancers. The mechanism of ROS-mediated anticancer activities of ginsenosides varies depending on the specific type of cancer cells involved. Ginsenosides may suppress cancer cell proliferation through anti-oxidation on tumor initiation and induce apoptosis, paraptosis or autophagy via generation of ROS on tumor progression, promotion, angiogenesis, invasion and metastasis by various signaling pathways e.g., activation of AMPK, MEK, ASK-1/JNK, ESR2-NCF1-ROS, ER-dependent PI3K/Akt/Nrf2, P53-CHOP, ROS-JNK-autophagy, and/or inhibition of PI3K/Akt signaling pathways. These multiple effects rather than a single may play a crucial role in emerging ginsenosides as a successful anticancer drug.
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