Prevention effect of rare ginsenosides against stress-hormone induced MTOC amplification

Cho, Jung-Hyun; Chun, Ho Young; Lee, Jung Suk; Lee, Jee Hyun; Cheong, Kyu Jin; Jung, Youn-Sang; Woo, Tae Gyun; Yoon, Min Ho; Oh, Ah Young; Kang, So‐mi; Lee, Chunghui; Sun, Hokeun; Hwang, Jihwan; Song, Gyu Yong; Park, Bum-Joon

doi:10.18632/oncotarget.9059

Cited by 15 publications

(6 citation statements)

References 43 publications

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“…We recently developed a technique for the mass production of the rare ginsenoside Rg6 from the ginsenoside Re, which is a main component of ginseng leaves 50 . Using this method, Rg6 was sufficiently prepared, and our group reported its effects on tumorigenesis 51 .…”

Section: Discussionmentioning

confidence: 99%

Rg6, a rare ginsenoside, inhibits systemic inflammation through the induction of interleukin-10 and microRNA-146a

Paik

Choe

Choi

et al. 2019

Sci Rep

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The immunobiological functions of Rg6, a rare ginsenoside from ginseng, have been largely unreported. In this paper, we demonstrate that Rg6 has a significant immunosuppressive function on Toll-like receptor (TLR) 4-induced systemic inflammatory responses. Rg6 was found to negatively regulate pro-inflammatory responses and severity in vivo, and thus induced recovery in mice with lipopolysaccharide (LPS)-induced septic shock and cecal ligation and puncture (CLP)-induced sepsis. Rg6 treatment also facilitated recovery in mice with LPS-induced lung damage via reduced neutrophil infiltration and tumor necrosis factor-α expression in lung tissues. Rg6 injection also downregulated pro-inflammatory cytokines and increased the levels of interleukin (IL)-10 in the serum of septic mice. Mechanistically, Rg6 did not induce TLR negative regulators, such as A20 and IRAK-M, in bone marrow-derived macrophages (BMDMs). Instead, addition of Rg6 to LPS-activated BMDMs augmented IL-10 expression, whereas it inhibited inflammatory signaling, such as by nuclear factor κB activation and mitogen-activated protein kinases. Furthermore, Rg6 significantly induced miR-146a, an operator miRNA for anti-inflammation, in BMDMs. Collectively, these data indicate that Rg6 inhibits inflammatory responses through the induction of IL-10 and miR-146a.

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Section: Discussionmentioning

confidence: 99%

Rg6, a rare ginsenoside, inhibits systemic inflammation through the induction of interleukin-10 and microRNA-146a

Paik

Choe

Choi

et al. 2019

Sci Rep

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“…This, in turn, inhibits the activation of proliferative signals in breast cancer cells [ 90 ]. Another study found [ 91 ] that intervention of Rg6 could block cortisol/cortisone-induced deregulation of microtubule organizing centers as well as ER signaling in breast cancer cells, alter stress hormone or steroid hormone-induced chromosomal instability, and inhibit aberrant activation of tumor cell proliferative signaling. The stress hormone cortisol and cortisone have been shown to elevate the expression of γ-tubulin, increasing the number of microtubule organizing centers and promoting resistance to paclitaxel in breast cancer cells.…”

Section: Mechanism Of Action Of Ginsenosides Altering Breast Cancer H...mentioning

confidence: 99%

“…Furthermore, Rg1 [ 120 ] has been demonstrated to inhibit the phosphorylation of histone H3Thr3 mediated by Haspin kinase, leading to an increase in the width of the metaphase plate and spindle instability during cancer cell division, resulting in a delay in the progression of mitotic differentiation and inhibition of proliferation in breast cancer cells. Similarly, intervention with Rg6 [ 91 ] can induce chromosomal instability, which resensitizes paclitaxel-resistant breast cancer cells to paclitaxel treatment.…”

Section: Mechanism Of Action Of Ginsenosides Altering Breast Cancer H...mentioning

confidence: 99%

Ginsenosides: changing the basic hallmarks of cancer cells to achieve the purpose of treating breast cancer

Jiang,

Fang,

Zhang

et al. 2023

Chin Med

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In 2021, breast cancer accounted for a substantial proportion of cancer cases and represented the second leading cause of cancer deaths among women worldwide. Although tumor cells originate from normal cells in the human body, they possess distinct biological characteristics resulting from changes in gene structure and function of cancer cells in contrast with normal cells. These distinguishing features, known as hallmarks of cancer cells, differ from those of normal cells. The hallmarks primarily include high metabolic activity, mitochondrial dysfunction, and resistance to cell death. Current evidence suggests that the fundamental hallmarks of tumor cells affect the tissue structure, function, and metabolism of tumor cells and their internal and external environment. Therefore, these fundamental hallmarks of tumor cells enable tumor cells to proliferate, invade and avoid apoptosis. Modifying these hallmarks of tumor cells represents a new and potentially promising approach to tumor treatment. The key to breast cancer treatment lies in identifying the optimal therapeutic agent with minimal toxicity to normal cells, considering the specific types of tumor cells in patients. Some herbal medicines contain active ingredients which can precisely achieve this purpose. In this review, we introduce Ginsenoside's mechanism and research significance in achieving the therapeutic effect of breast cancer by changing the functional hallmarks of tumor cells, providing a new perspective for the potential application of Ginsenoside as a therapeutic drug for breast cancer.

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“…Rg4, a rare ginsenoside, is the main low-polarity protopanaxatriol-type ginsenoside of black ginseng. Recently, the rare ginsenoside Rg4 was shown to exhibit potent antistress, antisubstrate metalloproteinase-13 expression, pulmonary protection, and apoptosis-inducing effects [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Activities of Rare Ginsenoside Rg4 on Cecal Ligation and Puncture-Induced Sepsis

Kim

Song

et al. 2022

IJMS

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Sepsis is an uncontrolled response to inflammatory infection and is associated with high levels of mortality and morbidity. Rg4 is a rare ginsenoside mainly found in the leaves of Panax ginseng C. A. Meyer and the major protopanaxatriol-type ginsenoside of black ginseng. In this study, we determined whether Rg4 affects cecal ligation and puncture (CLP)-induced sepsis. Animals were separated into the following six groups: control group, CLP-operated group, CLP plus maslinic acid (MA), and CLP plus Rg4 (5, 10, or 15 mg/kg). Survival rate, body weight changes, inflammatory cytokines, and histological analyses were assessed. Human endothelial cells were activated with the high-mobility group box 1 (HMGB1) protein and Rg4. Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assay (ELISA) and Western blot analysis were used to assess inflammation and gene expression, respectively. After CLP surgery, the Rg4-administered group exhibited a higher survival rate and body weight compared with the untreated control group. Rg4 treatment reduced cytokine levels, including tumor necrosis factor (TNF)-α and interleukin (IL)-1β, as well as nitric oxide (NO) levels and renal inflammation. After Rg4 treatment of HMGB1-activated cells, the expressions of toll-like receptor (TLR) 4 and TNF-α were decreased, and the activation of phosphoinositide 3-kinase (PI3K)/AKT signaling increased cell viability. In summary, Rg4 inhibited inflammation and exhibited a protective effect against CLP-induced sepsis, thereby reinforcing cell survival against septic responses.

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Prevention effect of rare ginsenosides against stress-hormone induced MTOC amplification

Cited by 15 publications

References 43 publications

Rg6, a rare ginsenoside, inhibits systemic inflammation through the induction of interleukin-10 and microRNA-146a

Rg6, a rare ginsenoside, inhibits systemic inflammation through the induction of interleukin-10 and microRNA-146a

Ginsenosides: changing the basic hallmarks of cancer cells to achieve the purpose of treating breast cancer

Inhibitory Activities of Rare Ginsenoside Rg4 on Cecal Ligation and Puncture-Induced Sepsis

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