Ginsenoside Rh2 suppresses growth of uterine leiomyoma in vitro and in vivo and may regulate ERα/c-Src/p38 MAPK activity

Zhu, Yinsu; Xu, Junjiu; Zhao, Li; Xie, Shuwu; Zhou, Jieyun; Guo, Xiangjie; Zhou, Xianying; Li, Guoting; Zhong, Ruiqin; Ma, Aiqun

doi:10.1016/j.jff.2015.06.057

Cited by 11 publications

(7 citation statements)

References 29 publications

(50 reference statements)

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“…The ginsenoside Rh 2 could suppress proliferation in several cancer cells, including human breast cancer (MCF-7) [77], lung cancer adenocarcinoma (A549 cells) [78], human colorectal carcinoma (HCT116) [79], prostate cancer (LNCaP and PC3) [56]. Leukemia (HL-60) [80], uterine leiomyoma [81], neuroblastoma (SK-N-BE-2) [82], glioblastoma multiforme (GBM) [83], human gastric cancer (SGC-7901) [84], hepatocellular carcinoma (HPEG-2) [85], intestinal (Int-407 and Caco-2) [86] and mouse melanoma (B16) [87].…”

Section: Pharmacological Studiesmentioning

confidence: 99%

Black Ginseng and Its Saponins: Preparation, Phytochemistry and Pharmacological Effects

et al. 2019

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Black ginseng is a type of processed ginseng that is prepared from white or red ginseng by steaming and drying several times. This process causes extensive changes in types and amounts of secondary metabolites. The chief secondary metabolites in ginseng are ginsenosides (dammarane-type triterpene saponins), which transform into less polar ginsenosides in black ginseng by steaming. In addition, apparent changes happen to other secondary metabolites such as the increase in the contents of phenolic compounds, reducing sugars and acidic polysaccharides in addition to the decrease in concentrations of free amino acids and total polysaccharides. Furthermore, the presence of some Maillard reaction products like maltol was also engaged. These obvious chemical changes were associated with a noticeable superiority for black ginseng over white and red ginseng in most of the comparative biological studies. This review article is an attempt to illustrate different methods of preparation of black ginseng, major chemical changes of saponins and other constituents after steaming as well as the reported biological activities of black ginseng, its major saponins and other metabolites.

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Section: Pharmacological Studiesmentioning

confidence: 99%

Black Ginseng and Its Saponins: Preparation, Phytochemistry and Pharmacological Effects

et al. 2019

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“…Furthermore, it has been reported that 20(S)-GRh2 exhibits stronger anticancer activity than 20(R)-GRh2 [ 17 – 18 ]. Due to its safety and no side-effects, GRh2 could be further developed as a useful drug for cancer therapy [ 19 , 20 ]. Recently, researchers have found that 20(S)-GRh2 could induce autophagy when undergoing induced apoptosis in Hepatocellular carcinoma [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of autophagy potentiates anticancer property of 20(S)-ginsenoside Rh2 by promoting mitochondria-dependent apoptosis in human acute lymphoblastic leukaemia cells

Xia

Wang

et al. 2016

Oncotarget

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Acute lymphoblastic leukaemia (ALL) is the most prevalent childhood malignancy. Although most children with ALL are cured, there is still a group of patients for which therapy fails owing to severe toxicities and drug resistance. Ginsenoside Rh2 (GRh2), a major bioactive component isolated from Panax ginseng, has been shown to have a therapeutic effect on some tumors. However, the molecular mechanisms of cell death induced by 20(S)-GRh2 in ALL cells remains unclear. In this study, we showed that 20(S)-GRh2 inhibited the cell growth and induced mitochondria-dependent apoptosis and autophagy. But it has no cytotoxic effect on human normal blood cells. Furthermore, autophagy plays a protective role in 20(S)-GRh2-induced apoptosis in ALL cell lines and human primary ALL cells. We demonstrated that either genetic or pharmacologic inhibition of autophagy could be more effective in reducing viability and enhancing 20(S)-GRh2-induced toxicity than 20(S)-GRh2 treatment alone. In addition, inhibition of autophagy could aggravate mitochondrial ROS generation and mitochondrial damage, and then accelerate mitochondria-dependent apoptosis. Taken together, these results suggest that inhibition of autophagy can sensitize ALL cells towards 20(S)-GRh2. The appropriate inhibition of autophagy could provide a powerful strategy to increase the potency of 20(S)-GRh2 as a novel anticancer agent for ALL therapy.

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“…A great quantity of researches have shown that ginsenosides can accelerate apoptosis, restrain proliferation, metastasis and angiogenesis, and promote immunity in various cancer cells. Zhu et al [16] in vivo and in vitro study of uterine fibroids found that ginsenoside Rh2 could inhibit the growth of rat uterine fibroids, and reduce serum hormone levels in a dose-dependent manner. With ELISA, qRT-PCR and Western blot detection of uterine fibroid cells confirmed that Rh2 decreased estrogen receptor alpha (ERa) and c-Src activity, increased p38 MAPK activity, reversed the ERa activity induced by PP2 and SB203580 (specific inhibitors of c-Src and p38 MAPK), which revealed the anti-proliferative effect of Rh2 and might be involved in the regulation of ERa/Src/p38 MAPK activity.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rb1 inhibits proliferation and promotes apoptosis by regulating HMGB1 in uterine fibroid cells

Zhang

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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To study the effects of ginsenoside Rb1 and the molecular mechanisms on proliferation and apoptosis of uterine fibroid cells, Rb1 þ pc DNA3.1, Rb1 þ pc DNA3.1-HMGB1, si-NC or si-HMGB1 was transfected into uterine fibroid cells by liposome method; the inhibitory rate and proliferation of human uterine fibroid cells were detected by MTT assay; apoptosis of uterine fibroid cells was detected by flow cytometry assay; HMGB1 protein expression in uterine fibroid cells was detected by Western blot assay. Compared with untreated uterine fibroid cells, the inhibitory and apoptosis rate of uterine fibroid cells treated with Rb1 were significantly up-regulated, while the expression level of HMGB1 was significantly down-regulated (p < .05). HMGB1 knockdown inhibited proliferation and promoted apoptosis of uterine fibroid cells. HMGB1 overexpression reversed the inhibitory effect on proliferation and the promotion effect on apoptosis of Rb1 in uterine fibroid cells. Ginsenoside Rb1 could inhibit uterine fibroid cells proliferation and promote apoptosis. This mechanism might be directly related to the downregulation of HMGB1, providing a basis for the treatment of uterine fibroids with ginsenoside Rb1. ARTICLE HISTORY

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Ginsenoside Rh2 suppresses growth of uterine leiomyoma in vitro and in vivo and may regulate ERα/c-Src/p38 MAPK activity

Cited by 11 publications

References 29 publications

Black Ginseng and Its Saponins: Preparation, Phytochemistry and Pharmacological Effects

Black Ginseng and Its Saponins: Preparation, Phytochemistry and Pharmacological Effects

Inhibition of autophagy potentiates anticancer property of 20(S)-ginsenoside Rh2 by promoting mitochondria-dependent apoptosis in human acute lymphoblastic leukaemia cells

Ginsenoside Rb1 inhibits proliferation and promotes apoptosis by regulating HMGB1 in uterine fibroid cells

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