Cyclovirobuxine D (CVB-D) is the main active component of the traditional Chinese medicine Buxus microphylla. Cyclovirobuxine D induces autophagy and attenuates the phosphorylation of Akt and mTOR[1]. Cyclovirobuxine D inhibits cell proliferation of gastric cancer cells through suppression of cell cycle progression and inducement of mitochondria-mediated apoptosis[2]. Cyclovirobuxine D is beneficial for heart failure induced by myocardial infarction[3].
Cyclovirobuxine D (0-240 µM ;24-72 hours) shows a concentration- and time-dependent reduced cell viability after CVB-D treatment, only 10% MGC-803 cells and 20% MKN28 cells are alive at 72 h after treatment with 240 µM[2].Cyclovirobuxine D (0-120 µM; 48 hours) arrests the cell cycle of gastric cancer cells at S phase in a concentration-dependent manner[2].Cyclovirobuxine D (0-120 µM; 48 hours) leads to apoptosis in gastric cancer cells in a concentration-dependent manner, especially early stage apoptosis.Cyclovirobuxine D (0-120 µM; 48 hours) causes apoptosis via up-regulation of the apoptosis- related proteins, cleaved Caspase-3 and ratio of Bax/Bcl-2, in gastric cancer cells[2]. Cell Viability Assay[2] Cell Line: MGC-803 and MKN28 cells
[1]. Lu J, et al. Cyclovirobuxine D induces autophagy-associated cell death via the Akt/mTOR pathway in MCF-7 human breast cancer cells. J Pharmacol Sci. 2014;125(1):74-82. Epub 2014 Apr 24. [2]. Wu J, et al. Cyclovirobuxine D Inhibits Cell Proliferation and Induces Mitochondria-Mediated Apoptosis in Human Gastric Cancer Cells. Molecules. 2015 Nov 19;20(11):20659-68. [3]. Yu B, et al. Beneficial effect of Cyclovirobuxine D on heart failure rats following myocardial infarction. Fitoterapia. 2011 Sep;82(6):868-77.