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Research: TAKEDA and colleagues,
Listed in Issue 66
Abstract
TAKEDA and colleagues, Second Department of Internal Medicine, Yamagata University School of Medicine, Japan aimed to determine the growth inhibition and induction of apoptotic cell death due to the herb Anemarrhena asphodeloides Bunge in gastric cancer cell lines and to clarify the mechanism of apoptosis.
Background
Methodology
Water-soluble ingredients of A. asphodeloides and the gastric cancer cell lines MKN45 and KATO-III were used in vitro. Measures of growth inhibition, induction of cell death, morphological features, the presence of DNA ladders, increases in caspase-3-like activity, the effects of a caspase-3 inhibitor on apoptotic cell death, and the release cytochrome C by A. asphodeloides were analyzed.
Results
A. asphodeloides inhibited the growth and decreased the viability of the gastric cancer cell lines . Low concentrations of A. asphodeloides resulted in greater viability of normal skin fibroblasts than of gastric cancer cells. A. asphodeloides induced apoptotic bodies and DNA ladders in MKN45 and KATO-III cells and increased caspase 3-like activity in MKN45 and KATO-III cells. The caspase 3 inhibitor Ac-DEVD-CHO inhibited the apoptotic cell death of gastric cancer cells induced by A. asphodeloides. Addition of A. asphodeloides caused cytochrome C to be released from mitochondria into the cytosol after 8 hours; cytochrome C levels reached a peak at 16 hours. Peak cytochrome C release was reached earlier than that of caspase 3-like activity.
Conclusion
The authors concluded that A. asphodeloides inhibited the growth of the gastric cancer cell lines MKN45 and KATO-III and induced apoptosis . The apoptosis of MKN45 and KATO-III cells induced by A. asphodeloides was associated with the release of cytochrome C from mitochondria, followed by an increase in caspase 3-like activity .
References
Takeda Y et al. Growth inhibition and apoptosis of gastric cancer cell lines by Anemarrhena asphodeloides Bunge. Journal of Gastroenterology 36 (2): 79-90. Feb 2001.
