Growth Inhibition and Induction of Apoptosis in NB4 Promyelocytic Leukemia Cells by Trypsin Inhibitor from Sweet Potato Storage Roots
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- 作者：Guan-Jhong Huang ; Ming-Jyh Sheu ; Hsien-Jung Chen ; Yuan-Shiun Chang ; Yaw-Huei Lin
- 刊名：Journal of Agricultural and Food Chemistry
- 出版年：2007
- 出版时间：April 4, 2007
- 年：2007
- 卷：55
- 期：7
- 页码：2548 - 2553
- 全文大小：248K
- 年卷期：v.55,no.7(April 4, 2007)
- ISSN：1520-5118
文摘
The objective of this study was to investigate the antiproliferative effect and the mechanism of trypsininhibitor (TI) from sweet potato [Ipomoea batatas (L.) Lam. 'Tainong 57'] storage roots on NB4promyelocytic leukemia cells. The results showed that TI inhibited cellular growth of NB4 promyelocyticleukemia cells in a time-dependent and dose-dependent manner, and treatment for 72 h induced amarked inhibition of cellular growth, showing an IC50 of 57.1 ± 8.26 
g/mL. TI caused cell cyclearrest at the G1 phase as determined by flow cytometric analysis and apoptosis as shown by DNAladdering. TI-induced cell apoptosis involved p53, Bcl-2, Bax, and cytochrome c protein in NB4 cells.P53 and Bax proteins were accumulated, and antiapoptotic molecule Bcl-2 was decreased in thetested cells in a time-dependent manner during TI treatment. TI also induced a substantial releaseof cytochrome c from the mitochondria into the cytosol. Hence, TI induced apoptosis in NB4 cellsthrough a mitochondria-dependent pathway, which was associated with the activation of caspase-3and -8. These results demonstrated that TI induces NB4 cell apoptosis through the inhibition of cellgrowth and the activation of the pathway of caspase-3 and -8 cascades.
g/mL. TI caused cell cyclearrest at the G1 phase as determined by flow cytometric analysis and apoptosis as shown by DNAladdering. TI-induced cell apoptosis involved p53, Bcl-2, Bax, and cytochrome c protein in NB4 cells.P53 and Bax proteins were accumulated, and antiapoptotic molecule Bcl-2 was decreased in thetested cells in a time-dependent manner during TI treatment. TI also induced a substantial releaseof cytochrome c from the mitochondria into the cytosol. Hence, TI induced apoptosis in NB4 cellsthrough a mitochondria-dependent pathway, which was associated with the activation of caspase-3and -8. These results demonstrated that TI induces NB4 cell apoptosis through the inhibition of cellgrowth and the activation of the pathway of caspase-3 and -8 cascades.