Ginsenoside Rg1 Induces Apoptosis through Inhibition of the EpoR-Mediated JAK2/STAT5 Signalling Pathway in the TF-1/Epo Human Leukemia Cell Line

Li, Jing; Wei, Qiang; Zuo, Guo‐Wei; Xia, Jing; You, Zhimei; Li, Chunli; Chen, Dilong

doi:10.7314/apjcp.2014.15.6.2453

Cited by 28 publications

(15 citation statements)

References 25 publications

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“…In terms of its positive effects, ginsenoside Rg1 reportedly has neurotropic and neuroprotective effects, counters oxidation and MPTP‐ or H 2 O 2 ‐induced apoptosis in neurons, stimulates differentiation and proliferation in human dental pulp cells and several mammalian cell lines, protects the cardiovascular system by decreasing oxidation and preventing apoptosis, and ameliorates diabetic cardiomyopathy by preventing ER stress‐induced apoptosis in diabetic rats . However, ginsenoside Rg1 has also been shown to inhibit cell proliferation and induce cell apoptosis, such as in the TF‐1/Epo human leukemia cell line . Although the latter finding suggests that ginsenoside Rg1 could be used to prevent and/or treat leukemia, the mechanisms through which ginsenoside Rg1 can inhibit/induce cell proliferation and apoptosis are unclear and warrant a detailed investigation.…”

Section: Discussionmentioning

confidence: 99%

“…It is known that chemical or physical injury can affect the complex and precisely orchestrated process of normal embryonic development, causing malformation or miscarriage during preimplantation and postimplantation embryogenesis. Given the conflicting reports indicating that ginsenoside Rg1 may induce or prevent cell apoptosis, it is very important to examine whether this compound has potential teratogenic effects on embryonic development. In this study, we show that incubation of mouse blastocysts with ginsenoside Rg1 for 24 h induced apoptosis in blastocysts and decreased the number of ICM cells, but had no effect on TE cells.…”

Section: Discussionmentioning

confidence: 99%

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Impairment of preimplantation and postimplantation embryonic development through intrinsic apoptotic processes by ginsenoside Rg1in vitroandin vivo

Anggelia

Chan

2017

Environmental Toxicology

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Ginsenoside Rg1, which is the most abundant compound found in Asian ginseng (Panax ginseng), has demonstrated various pharmacological actions, including neuroprotective, immune-stimulatory, and antidiabetic effects. Pregnant women, especially in the Asian community, consume ginseng as a nutritive supplement. Thus, the effects of ginsenoside-Rg1 on embryonic development need to be investigated, such as in a mouse model. As previous investigations have found that ginsenoside Rg1 appears to either trigger or prevent apoptosis in different cell lines, the effects of this agent on apoptosis remain to be clarified. In this study, we investigated whether ginsenoside Rg1 exerts a hazardous effect on mouse blastocysts and/or affects subsequent embryonic development in vitro and in vivo. Blastocysts treated with 25-100 μM ginsenoside Rg1 exhibited significant induction of apoptosis and a corresponding decrease in the inner cell mass (ICM) cell number. Importantly, the implantation rate was lower among ginsenoside Rg1-treated blastocysts compared to untreated controls. Moreover, embryo transfer assays revealed that blastocysts treated with 100 μM ginsenoside Rg1 exhibited increased resorption of postimplantation embryos and decreased weight among surviving fetuses. In vivo, intravenous injection of mice with ginsenoside Rg1 (2, 4, or 6 mg/kg body weight/day) for 4 days was associated with increased apoptosis of blastocyst-stage embryos and negatively impacted early embryonic development. Further experiments revealed that these effects may reflect the ability of ginsenoside Rg1 to trigger oxidative stress-mediated intrinsic apoptotic signaling. Our in vitro results indicate that ginsenoside　Rg1 treatment increases intracellular oxidative stress, decreases mitochondrial membrane potential, increases the Bax/Bcl-2 ratio, and activates caspase-9 and caspase-3, but not caspase-8. Taken together, our study results strongly suggest that ginsenoside Rg1 induces apoptosis and impairs the early preimplantation and postimplantation development of mouse embryos, both in vitro and in vivo.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Impairment of preimplantation and postimplantation embryonic development through intrinsic apoptotic processes by ginsenoside Rg1in vitroandin vivo

Anggelia

Chan

2017

Environmental Toxicology

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“…To date, more than 40 ginsenoside compounds have been identified [25]. Some of them, Rg1, Rg3, Rh1 and Rh2, for example, show the potent anticancer activity [24], [26]–[28]. Ginsenoside Rg3, a bioactive extracts of Panax ginseng , has various medical effects, such as anti-tumor [29]–[32], anti-oxidant, anti-inflammation properties [33], [34], inhibiting scar hyperplasia of skin [35] and angiogenesis [36].…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside 20(S)-Rg3 Targets HIF-1α to Block Hypoxia-Induced Epithelial-Mesenchymal Transition in Ovarian Cancer Cells

et al. 2014

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The prognosis of patients with ovarian cancer has remained poor mainly because of aggressive cancer progression. Since epithelial-mesenchymal transition (EMT) is an important mechanism mediating invasion and metastasis of cancer cells, targeting the EMT process with more efficacious and less toxic compounds to inhibit metastasis is of great therapeutic value for the treatment of ovarian cancer. We have found for the first time that the ginsenoside 20(S)-Rg3, a pharmacologically active component of the traditional Chinese herb Panax ginseng, potently blocks hypoxia-induced EMT of ovarian cancer cells in vitro and in vivo. Mechanistic studies confirm the mode of action of 20(S)-Rg3, which reduces the expression of hypoxia-inducible factor 1α (HIF-1α) by activating the ubiquitin-proteasome pathway to promote HIF-1α degradation. A decrease in HIF-1α in turn leads to up-regulation, via transcriptional suppression of Snail, of the epithelial cell-specific marker E-cadherin and down-regulation of the mesenchymal cell-specific marker vimentin under hypoxic conditions. Importantly, 20(S)-Rg3 effectively inhibits EMT in nude mouse xenograft models of ovarian cancer, promising a novel therapeutic agent for anticancer therapy.

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“…TGF-β1 (5 ng/ml) also significantly upregulated the expression of the mesenchymal marker vimentin, downregulated the expression of the epithelial marker E-cadherin and promoted invasion and migration of HepG2 cells. Previous studies have demonstrated that ginsenoside Rg1 may exert anti-cancer properties (13,18,26,27), however, this is the first study, to the best of our knowledge, to demonstrate that ginsenoside Rg1 may be a potential inhibitor of invasion and migration. The results of the transwell and wound-healing assays demonstrated that ginsenoside Rg1 inhibited TGF-β1-induced cell invasion and migration in HepG2 cells.…”

Section: Discussionmentioning

confidence: 61%

Ginsenoside Rg1 attenuates invasion and migration by inhibiting transforming growth factor-β1-induced epithelial to mesenchymal transition in HepG2 cells

Guo

et al. 2014

Molecular Medicine Reports

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Ginseng has become one of the most commonly used alternative herbal medicines and its active component, ginsenoside Rg1, possesses known pharmacological effects, including anticancer properties. However, the effects of ginsenoside Rg1 on metastasis have not been investigated. The present study demonstrated that ginsenoside Rg1 was able to suppress transforming growth factor‑β1 (TGF‑β1)‑induced invasion and migration in HepG2 liver cancer cells. This suppression was associated with the inhibition of TGF‑β1‑induced epithelial to mesenchymal transition (EMT). Furthermore, TGF‑β1 induced HepG2 cells to undergo EMT and significantly promoted cell invasion and migration. When cells were pretreated with ginsenoside Rg1 for 24 h and subsequently exposed to TGF‑β1 for 24 h, the results demonstrated that ginsenoside Rg1 inhibited the initiation of TGF‑β1‑induced EMT. In addition, HepG2 cells exhibited a mesenchymal phenotype when exposed to TGF‑β1, but when exposed to ginsenoside Rg1 this effect was reversed and the cells exhibited a classical epithelial morphology. Ginsenoside Rg1 also increased the expression of the epithelial phenotype marker E‑cadherin and repressed the expression of the mesenchymal phenotype marker vimentin. In conclusion, the results of the present study suggest that ginsenoside Rg1 may suppress liver cancer invasion and migration in vitro through inhibiting TGF‑β1‑induced EMT.

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Ginsenoside Rg1 Induces Apoptosis through Inhibition of the EpoR-Mediated JAK2/STAT5 Signalling Pathway in the TF-1/Epo Human Leukemia Cell Line

Cited by 28 publications

References 25 publications

Impairment of preimplantation and postimplantation embryonic development through intrinsic apoptotic processes by ginsenoside Rg1in vitroandin vivo

Impairment of preimplantation and postimplantation embryonic development through intrinsic apoptotic processes by ginsenoside Rg1in vitroandin vivo

Ginsenoside 20(S)-Rg3 Targets HIF-1α to Block Hypoxia-Induced Epithelial-Mesenchymal Transition in Ovarian Cancer Cells

Ginsenoside Rg1 attenuates invasion and migration by inhibiting transforming growth factor-β1-induced epithelial to mesenchymal transition in HepG2 cells

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