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Kong, Ah-Ng Tony,Yu, Rong,Chen, Chi,Mandlekar, Sandhya,Primiano, Thomas The Pharmaceutical Society of Korea 2000 Archives of Pharmacal Research Vol.23 No.1
Many natural products elicit diverse pharmacological effects. Using two classes of potential chemopreventive compounds, the phenolic compounds and the isothiocyanates, we review the potential utility of two signaling events, the mitogen-activated protein kinases (MAPKs) and the ICE/Ced-3 proteases (caspases) stimulated by these agents in mammalian cell lines. Studies with phenolic antioxidants (BHA, tBHQ), and natural products (flavonoids; EGCG, ECG, and isothiocyanates; PEITC, sulforaphane), provided important insights into the signaling pathways induced by these compounds. At low concentrations, these chemicals may activate the MAPK (ERK2, JNK1, p38) leading to gene expression of survival genes (c-Fos, c-Jun) and defensive genes (Phase II detoxifying enzymes; GST, QR) resulting in survival and protective mechanisms (homeostasis response). Increasing the concentrations of these compounds will additionally activate the caspase pathway, leading to apoptosis (potential cytotoxicity). Further increment to suprapharmacological concentrations will lead to nonspecific necrotic cell death. The wider and narrow concentration ranges between the activation of MAPK/gene induction and caspases/cell death exhibited by phenolic compounds and isothiocyanates, respectively, in mammalian cells, may reflect their respective therapeutic windows in vivo. Consequently, the studies of signaling pathways elicited by natural products will advance our understanding of their efficacy and safety, of which many man become important therapeuitc drugs of the future.
Red Ginseng Oil Inhibits TPA-Induced Transformation of Skin Epidermal JB6 Cells
Van-Long Truong,Ah-Ng Kong,정우식 한국식품영양과학회 2018 Journal of medicinal food Vol.21 No.4
Red ginseng oil (RGO) has been shown to possess anti-inflammatory and hepatoprotective activity. In this study, we evaluated the inhibitory effect of RGO on 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated neoplastic transformation of JB6 P+ cells. RGO pretreatment abolished the transformation of JB6 P+ cells challenged by TPA. RGO suppressed the transactivation of activator protein-1 (AP-1) and nuclear factor kappa B (NF-κB) transcription factors as well as protein levels of cyclooxygenase-2, cyclin D1, cyclin E, and Bcl-2 in the TPA-treated cells. Additionally, TPA-induced phosphorylations of extracellular signal-regulated kinases, 90 kDa ribosomal S6 kinase 2, c-Jun N-terminal kinases, and glycogen synthase kinase 3β were downregulated in the presence of RGO. Furthermore, RGO induced the nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant enzyme heme oxygenase-1 (HO-1) expression, and effectively blocked the overproduction of TPA-induced reactive oxygen species. These results suggest that RGO exerts a potent chemopreventive activity in skin cell model.
Kim, Hyo Jung,di Luccio, Eric,Kong, Ah-Ng Tony,Kim, Jong-Sang Wiley (John WileySons) 2011 BIOTECHNOLOGY JOURNAL Vol.6 No.5
<P>Numerous antioxidants have been reported to cause transcriptional activation of several antioxidant enzymes through binding antioxidant-response element on their promoter region. We, therefore, attempted to examine whether glyceollins, which share common structural features with many phase 2 enzyme inducers and antioxidant activity, could induce detoxifying/antioxidant enzymes. Glyceollins induced NAD(P)H:quinone oxidoreductase activity in a dose-dependent manner in both mouse hepatoma Hepa1c1c7 and its mutant BPRc1 cells. The compounds also increased the expression of some representative antioxidant enzymes, such as heme oxygenase 1,gamma-glutamylcysteine synthase, and glutathione reductase, by promoting nuclear translocation of the NF-E2-related factor-2 (Nrf2). Furthermore, phosphorylation of Akt and antioxidant response element-mediated reporter gene expression were enhanced by glyceollins but suppressed by LY294002, an inhibitor of phosphoinositide 3-kinases (PI3K). This suggests that glyceollins may cause Nrf2-mediated phase 2 enzyme induction through activation of the PI3K signaling pathway as well as interaction with Keap1. Our molecular docking simulations also suggest that the glyceollin isomers tightly bind into the binding pocket around Cys151, preventing Nrf2 from docking to Keap1. In conclusion, the current data suggest that glyceollins induced phase 2 detoxifying enzymes likely through promoting nuclear translocation of Nrf2, which is known to be regulated by phosphorylation of Nrf2 and/or disrupting Keap1-Nrf2 complex formation.</P>