Cytotoxic Activities of Flavonoid Glycoside Acetates from <i>Consolida oliveriana</i>

Dı́az, Jesús; Carmona, Armando J.; Torres, Fernando; Quintana, José; Estévez, Francisco; Herz, Werner

doi:10.1055/s-2008-1034278

Cited by 37 publications

(22 citation statements)

References 12 publications

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“…Natural compounds from fruits, vegetables, and grains, possess anti-cancer properties and represent a promising therapeutic approach for the prevention and treatment of many cancers [Kawasaki et al, 2008]. The anti-tumor activities of the natural compounds have recently attracted much attention [Diaz et al, 2008;Khan et al, 2008;Kim et al, 2010]. In the present study, we found that polydatin, a natural small compound, exhibited significant cytotoxicity in various human tumor cell lines.…”

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confidence: 52%

Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to polydatin-induced apoptosis in human nasopharyngeal carcinoma CNE cells

et al. 2011

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Previous studies revealed that polydatin, a natural small compound, possessed protective effect against ischemia/reperfusion injury and inflammation. However, the action and molecular mechanism of its potent anti-cancer activity remain poorly understood. In the present study, polydatin significantly killed several human tumor cell lines in a dose- and time-dependent manner. The compound also dose-dependently caused mitochondrial apoptosis in human nasopharyngeal carcinoma CNE cells. In addition, polydatin triggered endoplasmic reticulum (ER) stress and down-regulated the phosphorylation of Akt in CNE cells, while knock-down of CCAAT/enhancer-binding protein homologous protein (CHOP) dramatically abrogated the inactivation of Akt and reversed the pro-apoptotic effect of polydatin. Furthermore, polydatin provoked the generation of reactive oxygen species in CNE cells, while the antioxidant N-acetyl cysteine almost completely blocked the activation of ER stress and apoptosis, suggesting polydatin-induced reactive oxygen species is an early event that triggers ER stress mitochondrial apoptotic pathways in CNE cells. Taken together, these findings strongly suggest that polydatin might be a promising anti-tumor drug and our data provide the molecular theoretical basis for clinical application of polydatin.

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confidence: 52%

Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to polydatin-induced apoptosis in human nasopharyngeal carcinoma CNE cells

et al. 2011

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“…and UV/Visible spectroscopy and mass spectrometry). The details of the isolation have been published recently [13]. Stock solutions of 10 mM TA were made in dimethyl sulfoxide (DMSO) and aliquots were frozen at -20°C.…”

Section: Reagentsmentioning

confidence: 99%

“…1a), a flavonoid derivative which was obtained by acetylation of the natural product trifolin [13]. Antiproliferative studies on TA indicate that this compound displays similar cytotoxic properties in all cell lines assayed (IC 50 * 10 lM at 72 h).…”

Section: Ta Induces Apoptosis On Human Myeloid Leukaemia Cellsmentioning

confidence: 99%

“…The flavonoid trifolin (kaempferol-3-O-galactoside) has been isolated from the aerial parts of Consolida oliveriana [13]. We have previously shown that trifolin acetate (TA), obtained by acetylation of the natural product trifolin, is cytotoxic on human leukaemia-(HL-60 and U937) and melanoma-(SK-MEL-1) cell lines and displays similar potency among different cell lines [13]. Here we have studied the effect of this compound on apoptosis induction on the above tumor cell lines as well as human myeloid cells over-expressing the anti-apoptotic proteins Bcl-2 and Bcl-x L .…”

Section: Introductionmentioning

confidence: 99%

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Trifolin acetate-induced cell death in human leukemia cells is dependent on caspase-6 and activates the MAPK pathway

et al. 2008

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In the present study we demonstrated that the flavonoid derivative trifolin acetate (TA), obtained by acetylation of naturally occurring trifolin, induces apoptosis. Associated downstream signaling events were also investigated. TA-induced cell death was prevented by the non-specific caspase inhibitor z-VAD-fmk and reduced by the presence of the selective caspase inhibitors z-LEHD-fmk (caspase-9), z-DEVD-fmk (caspase-3) and z-VEID-fmk (caspase-6). The apoptotic effect of TA was associated with (i) the release of cytochrome c from mitochondria which was not accompanied by dissipation of the mitochondrial membrane potential (DeltaPsi(m)), (ii) the activation of the mitogen-activated protein kinases (MAPKs) pathway and (iii) abrogated by the over-expression of Bcl-2 or Bcl-x(L). TA-induced cell death was attenuated by inhibition of extracellular signal-regulated kinases (ERK) 1/2 with U0126 and inhibition of p38(MAPK) with SB203580. In contrast, inhibition of c-Jun NH(2)-terminal kinase (JNK) by SP600125 significantly enhanced apoptosis. Although reactive oxygen species (ROS) increased in response to TA, this did not seem to play a pivotal role in the apoptotic process since different anti-oxidants were unable to provide cell protection. The present study demonstrates that TA-induced cell death is mediated by an intrinsic-dependent apoptotic event involving mitochondria and MAPK, and through a mechanism independent of ROS generation.

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“…Flavonoids have recently gained attention due to their antitumor activity (9)(10)(11). Icaritin is a prenylflavonoid and is a hydrolytic product of icaritin, derived from Herba Epimedii.…”

Section: Introductionmentioning

confidence: 99%

Anticancer agent icaritin induces apoptosis through caspase-dependent pathways in human hepatocellular carcinoma cells

Sun

Peng

et al. 2014

Molecular Medicine Reports

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Abstract.Icaritin is an active ingredient derived from the plant Herba epimedium, which exhibits various pharmacological and biological activities. However, the function, and the underlying mechanisms of icaritin on the growth of SMMC-7721 human hepatoma cells have yet to be elucidated. The present study aimed to investigate the function and underlying mechanisms of icaritin in the growth of SMMC-7721 cells. The cells were treated with varying concentrations of icaritin for 12, 24 and 48 h, respectively, prior to cytotoxic analysis. Apoptosis of SMMC-7721 cells following treatment with icaritin was measured using flow cytometry. The gene expression of mitochondria-and Fas-mediated caspase-dependent pathways was detected by reverse transcription-quantitative polymerase chain reaction and western blotting. Statistical analysis was performed by Student's t-test and one-way analysis or variance. The present study demonstrated that treatment with icaritin significantly inhibited growth, and induced apoptosis of SMMC-7721 cells, in a time-and dose-dependent manner. In addition, icaritin triggered the mitochondrial/caspase apoptotic pathway, by decreasing the Bcl-2/Bax protein ratio and increasing activation of caspase-3. Icaritin also activated the Fas-mediated apoptosis pathway, as was evident by the increased expression levels of Fas and activation of caspase-8. These data suggest that icaritin may be a potent growth inhibitor and induce apoptosis of SMMC-7721 cells through the mitochondria-and Fas-mediated caspase-dependent pathways. The present study may provide experimental evidence for preclinical and clinical evaluations of icaritin for HCC therapy.

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Cytotoxic Activities of Flavonoid Glycoside Acetates from Consolida oliveriana

Cited by 37 publications

References 12 publications

Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to polydatin-induced apoptosis in human nasopharyngeal carcinoma CNE cells

Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to polydatin-induced apoptosis in human nasopharyngeal carcinoma CNE cells

Trifolin acetate-induced cell death in human leukemia cells is dependent on caspase-6 and activates the MAPK pathway

Anticancer agent icaritin induces apoptosis through caspase-dependent pathways in human hepatocellular carcinoma cells

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