Bufadienolides from animal and plant sources

Krenn, Liselotte; Kopp, Brigitte

doi:10.1016/s0031-9422(97)00426-3

Cited by 246 publications

(160 citation statements)

References 67 publications

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“…Bufalin is the major digoxin-like immunoreactive component of Chan Su, a traditional Chinese medicine obtained from the skin and parotid venom glands of the toad (Krenn and Kopp, 1998), the molecular formula of which is C24H34O4 with a relative molecular weight 386.5g/mol. The chemical structure of bufalin is shown in Figure 1A.…”

Section: Introductionmentioning

confidence: 99%

Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

Ding

Zhang²,

Huang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Background: To evaluate the effects of bufalin in A549 human lung adenocarcinoma epithelial cells in vitro and assess the underlying mechanisms. Materials and Methods: Human A549 non-small cell lung cancer (NSCLC) cells were treated with various concentrations of bufalin. Cell proliferation was measured by CCK-8 assay, apoptotic cell percentage was calculated by flow cytometry and morphological change was observed by inverted phase contrast microscopy/transmission electron microscopy. In addition, the membrane potential of mitochondria was detected by JC-1 fluorescence microscopy assay, and the related protein expression of cytochrome C and caspase-3 was analyzed by Western blotting. Results: Bufalin could inhibit the proliferation of A549 cells via induction of apoptosis, with the evidence of characteristic morphological changes in the nucleus and mitochondria. Furthermore, bufalin decreased the mitochondrial membrane potential with up-regulation of cytochrome C in the cytosol, and activation of caspase-3. Conclusions: Bufalin inhibits the proliferation of A549 cells and triggers mitochondria-dependent apoptosis, pointing to therapeutic application for NSCLC.

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Section: Introductionmentioning

confidence: 99%

Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

Ding

Zhang²,

Huang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…Bufalin is a traditional Chinese medicine and it is the major digoxin-like immunoreactive component of Chan Su, which is obtained from the skin and parotid venom glands of toads (1). It is a cardioactive C-24 steroid, with the molecular formula C 24 H 34 O 4 and a relative molecular weight of 386.5.…”

Section: Introductionmentioning

confidence: 99%

BMI-1 is important in bufalin-induced apoptosis of K562 cells

Lian

Wang

Wei

et al. 2014

Molecular Medicine Reports

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Abstract. The purpose of this study was to analyze the effects of bufalin on the gene expression of K562 cells and on the expression of BMI-1 pathway constituents in K562 cell apoptosis. K562 cells were treated with bufalin, and the inhibition rate and apoptosis were detected by an MTT assay, flow cytometry and a microarray assay. BMI-1, p16 INK4a and p14 ARF were examined by quantitative polymerase chain reaction (qPCR). Bufalin induced significant changes in the gene expression of the K562 cells; 4296 genes were differentially expressed, 2185 were upregulated and 2111 were downregulated. The most upregulated genes were associated with transcription regulation, while the most downregulated genes were associated with the non-coding RNA metabolic processes and DNA repair. qPCR analysis demonstrated that BMI-1 was overexpressed in the K562 cells. Bufalin is able to downregulate BMI-1 expression levels in K562 cells prematurely and cause an increase in the expression levels of p16 INK4a and p14 ARF . Moreover, bufalin downregulated BCR/ABL expression levels in a time-dependent manner, and the expression of BCR/ABL was not associated with the upregulation or downregulation of BMI-1 expression. Bufalin may induce K562 cell apoptosis by downregulating BMI-1 expression levels and accordingly upregulating the expression levels of p16 INK4a and p14 ARF . Bufalin may also induce K562 cell apoptosis via downregulating BCR/ABL expression levels, and this pathway may be independent of the BMI-1 pathway.

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“…Natural products, including those from plants and microorganisms, provide rich potential for anticancer drug discovery. The cinobufocini injection is a preparation containing water-soluble components of Chan Su, a traditional Chinese medicine obtained from the skin and parotid venom glands of the toad (2). The chemical formula of cinobufocini is shown in Fig.…”

Section: Introductionmentioning

confidence: 99%

“…1. Cinobufocini and other bufadienolides are cardioactive C-24 steroids that exhibit a variety of biological activities, such as cardiotonic, anesthetic and antineoplastic activities (2). Both clinical and laboratory studies showed that cinobufocini has anticancer effects (3,4); however, there is limited information on the global molecular mechanisms of cinobufocini action in lung cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Cinobufocini inhibits NF-κB and COX-2 activation induced by TNF-α in lung adenocarcinoma cells

et al. 2012

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Abstract. The aim of the present study was to investigate the effects of cinobufocini on nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2) and the production of cytokines induced by tumor necrosis factor-α (TNF-α) in the A549 cell line. A549 cells were incubated with cinobufocini at different concentrations for 24, 48 or 72 h. Cell proliferation was examined by the WST-8 assay. The expression of NF-κB, COX-2 and inhibitor κBα (IκBα) was studied by western blotting. The NF-κB-dependent luciferase rporter (3xκB-luc) was transfected for 24 h, the cells were treated with the reagents for 24 h, and the transcriptional activity of the NF-κB promoter was detected by a luciferase assay. The levels of IL-6 and IL-8 mRNA were detected by reverse transcription-polymerase chain reaction. We found that cinobufocini inhibited NF-κB p65 expression and the transcriptional activity of the NF-κB promoter induced by TNF-α compared with the control in the nuclei of A549 cells. Moreover, induced COX-2 expression was blocked by cinobufocini and was correlated with a reduction in the activated p65 subunit of NF-κB. Additionally, the levels of IL-6 and IL-8 mRNA induced by TNF-α were significantly suppressed by the addition of cinobufocini. In conclusion, these results suggest that the anti-inflammatory effects of cinobufocini are dependent on the NF-κB/COX-2 pathway in A549 cells, thereby providing a possible anticancer mechanism for the compound.

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Bufadienolides from animal and plant sources

Cited by 246 publications

References 67 publications

Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

BMI-1 is important in bufalin-induced apoptosis of K562 cells

Cinobufocini inhibits NF-κB and COX-2 activation induced by TNF-α in lung adenocarcinoma cells

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