Panax ginseng (ginseng)
(3β,12β)-12,20-Dihydroxydammar-24-en-3-yl β-D-glucopyranoside/β-D-Glucopyranoside, (3β,12β)-12,20-dihydroxydammar-24-en-3-yl/ginenoside Rh2/(3β,12β)-12,20-Dihydroxydammar-24-en-3-yl-β-D-glucopyranoside/dihydroxydammar-24-en-3-yl/β-D-Glucopyranoside, (3α,5ξ,9ξ,12α,13α,14β)-12,20-dihydroxydammar-24-en-3-yl/(2R,3R,4S,5S,6R)-2-[[(3R,8R,10R,12S,13S,14S,17S)-12-hydroxy-17-[(2S)-2-hydroxy-6-methylhept-5-en-2-yl]-4,4,8,10,14-pentamethyl-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-yl]oxy]-6-(hydroxymethyl)oxane-3,4,5-triol/Ginsenoside Rh2/GinsenosideRh2/(3α,5ξ,9ξ,12α,13α,14β)-12,20-Dihydroxydammar-24-en-3-yl β-D-glucopyranoside/Ginsenoside Rh2, 20(S)-
Ginsenoside Rh2 is isolated from the root of Ginseng. Ginsenoside Rh2 induces the activation of caspase-8 and caspase-9. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner.
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Acute myeloid leukemia (AML) and Chronic myelogenous leukemia (CML) are common leukemia in adults. 20(S)-GRh2 is an important bioactive substance that is present in Panax ginseng. However, there are no investigations that deal with the comparison of apoptosis, the occurrence of autophagy, and the relationship between apoptosis and autophagy after being treated with 20(S)-GRh2 in AML and CML. In this study, we explored the effect of 20(S)-GRh2 on the AML and CML (U937 and K562). Fluorescence microscopy, CCK-8, Quantitative realtime PCR, Western blot, transmission electron microscopy (TEM), and flow cytometric analysis were used to detect the occurrence of cell proliferation inhibition, apoptosis, and autophagy. By using the above methods, it was determined that apoptosis induced by 20(S)-GRh2 was more obvious in K562 than U937 cells and 20(S)-GRh2 could generate autophagy in K562 and U937 cells. When pretreated by a specific inhibitor of autophagy, (3-methyladenine), the 20(S)-GRh2-induced apoptosis was enhanced, which indicated that 20(S)-GRh2-induced autophagy may protect U937 and K562 cells from undergoing apoptotic cell death. On the other hand, pretreated by an apoptosis suppressor (Z-VAD-FMK), it greatly induced the autophagy and partially prevented 20(S)-GRh2 induced apoptosis. This phenomenon indicated that 20(S)-GRh2-induced autophagy may serve as a survival mechanism and apoptosis and autophagy could act as partners to induce cell death in a cooperative manner. These findings may provide a rationale for future clinical application by using 20(S)-GRh2 combined autophagy inhibitors for AML and CML.
20(S)-GRh2; AML; CML; apoptosis; autophagy; cooperative manner
20(S)-Ginsenoside Rh2 Induce the Apoptosis and Autophagy in U937 and K562 Cells.
Zhuang J1, Yin J2, Xu C3, Mu Y4, Lv S5.
2018 Mar 8
20(S)-Ginsenoside Rh2 (20(S)-GRh2) exerts important pharmacological effects with regard to the control of human hepatocellular carcinoma (HCC). EZH2 is a potent histone methyltransferase of H3K27me3, which has been determined as an oncogene in many malignancies. The CDKN2A-2B gene cluster encodes three important tumor suppressors, P14, P15 and P16. In this study, the anticancer effect and molecular mechanism of 20(S)-GRh2 on HCC was investigated. Treatment of HCC cells with 20(S)-GRh2 inhibited cell proliferation, migration and induced cell cycle arrest at the G0/G1 phase, and inhibited tumor growth in vivo. We demonstrate for the first time that this effect was specifically mediated by down-regulating expression of EZH2. Further molecular mechanism study indicated that the decreased EZH2 promoted P14, P15 and P16 gene transcription through reducing H3K27me3 modification in the promoter of CDKN2A-2B gene cluster loci. Similarly, silencing of EZH2 by siRNA down-regulated P14, P15, P16 mRNA levels and inhibited HCC cell proliferation. Our results suggested that EZH2 could be a potentially therapeutic target by 20(S)-GRh2 in HCC, which provided a rationale for the development of drugs that inhibited histone methylase as a strategy against various cancers.
Copyright ? 2017 Elsevier B.V. All rights reserved.
20(S)-Ginsenoside Rh2; CDKN2A-2B gene cluster; EZH2; Ginsenoside Rh2 (PubChem CID: 119307); Hepatocellular carcinoma
20(S)-Ginsenoside Rh2 suppresses proliferation and migration of hepatocellular carcinoma cells by targeting EZH2 to regulate CDKN2A-2B gene cluster transcription.
Li Q1, Li B2, Dong C3, Wang Y3, Li Q4.
2017 Nov 15
20(S)-ginsenoside Rh2 (Rh2), a well-known protopanaxadiol-type ginsenoside from Panax ginseng has especially gained attention for its anticancer activities on various types of human cancer cells. However, the molecular mechanism through which Rh2 promotes apoptosis in hepatocellular carcinoma (HePG2) cells is not known at the transcriptome level. Rh2 can specifically inhibit the proliferation of HePG2 in a dose- and time-dependent manner. Moreover, Rh2 can significantly increase the apoptosis which was related with an increase in protein expression levels of caspase-3, caspase-6, and poly (ADP-ribose) polymerase. Comparison of RNA-seq transcriptome profiles from control group and Rh2-treated group yielded a list of 2116 genes whose expression was significantly affected, which includes 971 up-regulated genes and 1145 down-regulated genes. The differentially expressed genes in p53 signaling pathway and DNA replication may have closely relationships to the cells apoptosis caused by Rh2 treatment. The results of qPCR validation showed that dynamic changes in mRNA, such as CDKN1A, CCND2, PMAIP1, GTSE1, and TP73.
Copyright ? 2019 Zhang, Li, Yuan, Zhou, Zhang, Cao, Fu and Hu.
20(S)-ginsenoside Rh2; RNA-seq; anti-proliferation; hepatocellular carcinoma; p53 signaling pathway
Transcriptome Analyses of the Anti-Proliferative Effects of 20(S)-Ginsenoside Rh2 on HepG2 Cells.
Zhang J1, Li W1, Yuan Q1, Zhou J1, Zhang J1, Cao Y1, Fu G2, Hu W1.
2019 Nov 7