Magnolol induces apoptosis in human leukemia cells via cytochrome c release and caspase activation

Wen Bin Zhong, Chih Yuan Wang, Kuo Jang Ho, Fung Jou Lu, Tien Chun Chang, Wen Sen Lee

研究成果: 雜誌貢獻文章同行評審

26 引文 斯高帕斯(Scopus)


Magnolol, isolated from the stem bark of Magnolia officnalis, was found to inhibit proliferation of human HL-60 cells and Jurkat T leukemia cells via inducing apoptosis in a dose- and time-dependent manner. By contrast, magnolol did not cause apoptosis in neutrophils and peripheral blood mononuclear cells of healthy donors. Apoptosis was determined by detection of DNA fragmentation in gel electrophoresis, morphological alternations by flow cytometry, quantification of phosphatidylserine externalization by Annexin V labeling and oligonucleosomal DNA content by TUNEL labeling. Activation of caspase-9, -3 and -2, and the proteolytic cleavage of poly(ADP-ribose) polymerase were found during apoptosis induced by magnolol. In addition, both pan-caspase and selective caspase-9 inhibitor blocked magnolol-induced apoptosis. The apoptosis could also be partially attenuated by caspase-3 and -2 inhibitors. Magnolol induced the reduction of mitochondrial transmembrane potential and the release of cytochrome c into cytoplasm. In conclusion, our findings indicate that magnolol-induced apoptotic signaling is carried out through mitochondria alternations to caspase-9 and that then the downstream effector caspases are activated sequentially. Magnolol could be a potentially effective drug for leukemia with low toxicity to Anti-normal blood cells and it merits further investigation.

頁(從 - 到)211-217
期刊Anti-Cancer Drugs
出版狀態已發佈 - 3月 2003

ASJC Scopus subject areas

  • 藥理
  • 癌症研究
  • 腫瘤科


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