Structure–function relationship exists for ginsenosides in reducing cell proliferation and inducing apoptosis in the human leukemia (THP-1) cell line

Popovich, David G.; Kitts, David D.

doi:10.1016/s0003-9861(02)00398-3

Cited by 189 publications

(115 citation statements)

References 23 publications

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“…Chronic intake of P ginseng decreased the incidence of lung, gastric, liver and colorectal tumors. Rh2 and Rg3 suppressed breast, prostate, liver and intestinal cancer [11,[48][49][50][51][52][53] . The anti-proliferative effects of petroleum ether extract of P ginseng in cultured human renal cell carcinoma cell lines were demonstrated; even its potency was weaker than partially purified P ginseng preparation, panaxydol, and some as panazynol [54] .…”

Section: Pharmacologymentioning

confidence: 99%

Comparison of the pharmacological effects ofPanax ginsengandPanax quinquefolium

Chen¹,

Chiou²,

Zhang

2008

Acta Pharmacologica Sinica

232

139

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Medical application of Panax ginseng was first found in "Shen-Nong Herbal Classic" around 200 AD Panax quinquefolium was first introduced in "Essential of Materia Medica" in 1694 in China. The most important bioactive components contained in P ginseng and P quinquefolium are ginseng saponins (GS). The contents of ginsenoside Rb1, Re, and Rd in P quinquefolium are higher than they are in P ginseng. In P ginseng, the contents of Rg1,Rb2, and Rc are higher than they are in P quinquefolium. P ginseng had a higher ratio of Rg1: Rb1, and which was lower in P quinquefolium. After steaming for several hours, the total GS will decrease. However, some ginsenosides (Rg2, 20R-Rg2, Rg3, Rh1 and Rh2) increase, while others (Rb1, Rb2, Rb3, Rc, Rd, Re, and Rg1) decrease. However, variation, especially in P quinquefolium, is high. P ginseng and P quinquefolium are general tonics and adaptogens. Rg1 and Rb1 enhance central nervous system (CNS) activities, but the effect of the latter is weaker. Thus, for the higher contents of Rg1, P ginseng is a stimulant, whereas the Rb1 contents of P quinquefolium are mainly calming to the CNS. Re, Rg1, panaxan A and B from P ginseng are good for diabetes. Re and Rg1 enhance angiogenesis, whereas Rb1, Rg3 and Rh2 inhibit it. Rh2, an antitumor agent, can be obtained from Rb1 by steaming. The content of Re in P quinquefolium are higher than in P ginseng by 3-4 times. The vasorelax, antioxidant, antihyperlipidemic, and angiogenic effects of Re are reported. Thus, for the CNS "hot," wound healing and hypoglycemic effects, P ginseng is better than P quinquefolium. For anticancer effects, P quinquefolium is better.

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Section: Pharmacologymentioning

confidence: 99%

Comparison of the pharmacological effects ofPanax ginsengandPanax quinquefolium

Chen¹,

Chiou²,

Zhang

2008

Acta Pharmacologica Sinica

232

139

View full text Add to dashboard Cite

show abstract

“…Some researches show that the ginseng was used not only to decrease proliferation of human cancer cells in vitro (Oh et al, 1999;Popovich et al, 2002), but also as an adjuvant to enhance efficacy and reduce side-effects of active cancer therapies such as chemotherapy and radiotherapy (Jia et al, 2009). How does the ginseng act its function to anti-cancer cells and what are the underling mechanisms with the anticancer effects interaction by ginseng?…”

Section: Introductionmentioning

confidence: 99%

Senescence as A Consequence of Ginsenoside Rg₁Response on K562 Human Leukemia Cell Line

Liu

Cai²,

Zhou³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Aims and Background: Traditional chemotherapy strategies for human leukemia commonly use drugs based on cytotoxicity to eradicate cancer cells. One predicament is that substantial damage to normal tissues is likely to occur in the course of standard treatments. Obviously, it is urgent to explore therapies that can effectively eliminate malignant cells without affecting normal cells. Our previous studies indicated that ginsenoside Rg 1 (Rg 1 ), a major active pharmacological ingredient of ginseng, could delay normal hematopoietic stem cell senescence. However, whether Rg 1 can induce cancer cell senescence is still unclear. Methods: In the current study, human leukemia K562 cells were subjected to Rg 1 exposure. The optimal drug concentration and duration with K562 cells was obtained by MTT colorimetric test. Effects of Rg 1 on cell cycle were analyzed using flow cytometry and by SA-β-Gal staining. Colony-forming ability was measured by colony-assay. Telomere lengths were assessed by Southern blotting and expression of senescence-associated proteins P21, P16 and RB by Western blotting. Ultrastructural morphology changes were observed by transmission electron microscopy. Results: K562 cells demonstrated a maximum proliferation inhibition rate with an Rg 1 concentration of 20 μ mol·L -1 for 48h, the cells exhibiting dramatic morphological alterations including an enlarged and flat cellular morphology, larger mitochondria and increased number of lysosomes. Senescence associated-β-galactosidase (SA-β-Gal) activity was increased. K562 cells also had decreased ability for colony formation, and shortened telomere length as well as reduction of proliferating potential and arrestin G 2 /M phase after Rg 1 interaction. The senescence associated proteins P21, P16 and RB were significantly up-regulated. Conclusion: Ginsenoside Rg 1 can induce a state of senescence in human leukemia K562 cells, which is associated with p21-Rb and p16-Rb pathways.

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“…Particular attention has been given to their potential for cancer chemoprevention, especially as apoptosis inducers (5)(6)(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of human rheumatoid arthritis synovial cell survival by hecogenin and tigogenin is associated with increased apoptosis, p38 mitogen-activated protein kinase activity and upregulation of cyclooxygenase-2

Liagre¹,

Vergne-Salle²,

Léger³

et al. 2007

Int J Mol Med

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Abstract. We conducted our study to assess the antiproliferative and proapoptotic potential of hecogenin and tigogenin, two saponins which are structurally similar to diosgenin. We particularly focused our attention on mitogenactivated protein kinase (MAPK) activation in relation to apoptosis but also with the COX-2 expression and activity. Rheumatoid arthritis (RA) synoviocytes were isolated from fresh synovial biopsies obtained from five RA patients undergoing hip arthroplasty. Measurement of cell proliferation was determined using the MTT assay. Apoptosis was evaluated by studying caspase-8, caspase-9 and caspase-3 activities but also by quantification of DNA fragmentation. Quantification of human phospho-MAPKs was realized by ELISA. COX-2 expression was demonstrated by Western blot analysis and COX-2 activity by assay of endogenous prostaglandin E 2 (PGE 2 ) production. Tigogenin was more effective than hecogenin in inducing apoptosis in human RA fibroblast-like synoviocytes (FLS) which was caspase dependent but poly(ADP-ribose) polymerase independent and characterized by DNA fragmentation. Our results demonstrated hecogenin-and tigogenin-induced apoptosis through activation of p38 without affecting the JNK and ERK pathways. Indeed, pretreatment with a p38 inhibitor decreased saponin-induced apoptosis with a significant decrease in DNA fragmentation. Furthermore, the rate of apoptosis induced by hecogenin or tigogenin was associated with overexpression of COX-2 correlated with overproduction of endogenous PGE 2 . These new results provide strong evidence that a family of structurally similar plant steroids is capable of inducing apoptosis in human RA FLS with different rates and different signalling pathways. This study also confirms the discussed appearance of the downregulation or upregulation of COX-2 in cell apoptosis as a function of cell type. IntroductionPlant steroids have been thoroughly described for their pharmacological properties, including hypocholesterolemic (1), antidiabetic (2) and antioxidant activities (3,4). Particular attention has been given to their potential for cancer chemoprevention, especially as apoptosis inducers (5-10).Apoptosis is considered to be one of the mechanisms regulating autoimmune diseases such as rheumatoid arthritis (RA) (11). In the pathogenesis of RA, it is thought that the normal balance between proliferation and apoptosis of synovial fibroblasts is lost, leading to hyperplasia of these fibroblasts (12). Activated synovial cells cause growth of synovium in the articular cavity along with angiogenesis, invade the adjacent bone, promote production of inflammatory mediators by inflammatory cells, and cause cartilage and bone destruction (13). Therefore, it has been shown that stimulation of apoptosis in synovial fibroblasts might be useful for the treatment of RA (14,15).We showed for the first time that a plant steroid, diosgenin, inhibited the growth of human RA fibroblast-like synoviocytes (FLS) with apoptosis induction characterized by a loss of mitochondrial me...

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Structure–function relationship exists for ginsenosides in reducing cell proliferation and inducing apoptosis in the human leukemia (THP-1) cell line

Cited by 189 publications

References 23 publications

Comparison of the pharmacological effects ofPanax ginsengandPanax quinquefolium

Comparison of the pharmacological effects ofPanax ginsengandPanax quinquefolium

Senescence as A Consequence of Ginsenoside Rg₁Response on K562 Human Leukemia Cell Line

Inhibition of human rheumatoid arthritis synovial cell survival by hecogenin and tigogenin is associated with increased apoptosis, p38 mitogen-activated protein kinase activity and upregulation of cyclooxygenase-2

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Structure–function relationship exists for ginsenosides in reducing cell proliferation and inducing apoptosis in the human leukemia (THP-1) cell line

Cited by 189 publications

References 23 publications

Comparison of the pharmacological effects ofPanax ginsengandPanax quinquefolium

Comparison of the pharmacological effects ofPanax ginsengandPanax quinquefolium

Senescence as A Consequence of Ginsenoside Rg1Response on K562 Human Leukemia Cell Line

Inhibition of human rheumatoid arthritis synovial cell survival by hecogenin and tigogenin is associated with increased apoptosis, p38 mitogen-activated protein kinase activity and upregulation of cyclooxygenase-2

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Senescence as A Consequence of Ginsenoside Rg₁Response on K562 Human Leukemia Cell Line