Dr. Zhang received B.S. of Pharmaceutical Sciences and M.S. of Pharmacognosy from Peking University, Ph.D. of Oncology in Sun Yat-sen University. He has been a visiting scholar at School of Chinese Medicine, Hong Kong Baptist University for two years. He is currently Committee Member of the Society of Anti-Cancer Drugs, Chinese Anti-Cancer Association and Committee Member of Division of Tumor Pharmacology, Chinese Pharmacological Society.


To observe the changes of mitochondrial membrane potential (MMP),cytochrome c (Cyto-c) , Caspase-3, 9 activity and cleavage of PARP, and determine the apoptosis signaling pathway in Bruceine D -treatment K562 cells. Method:MTT assay was used to evaluate the cell growth inhibition of Bruceine D in vitro; Flow cytometry were performed to analyze MMP; Western Blot analysis was applied to detect Cyto-c , Caspases-3,-9 and PARP in K562 cells. Results:IC50 value of Bruceine D against K562 cells was 6.37±0.39 μM. The percentages of MMP after the treatment of 3.0,6.0,12.0 μM Bruceine D for 24 h were 79.84 ± 4.46%, 59.74 ± 7.48%, 40.66 ± 4.37%(P<0.05)respectively . The release of Cyto-c, activity of Caspase-3, 9 and cleavage of PARP increased compared with the control groups in the Bruceine D induced K562 cell . Moreover, Bruceine D could decrease Phosphorylation level of AKT and ERK. Conclusions The collapse of MMP, the increased Cyto-c , the up-regulation of Caspase-3, -9 activity and the augmented cleavage of PARP emerged after K562 cells treated by Bruceine D. The apoptosis of K562 cells induced by Bruceine D might be related to the mitochondrial pathway of apoptosis. Reduction of AKT and ERK Phosphorylation level might be mechanism of growth inhibition of K562 cells mediated by Bruceine D.