Abstract | OBJECTIVE: METHODS: K562/ADR cells were treated with various concentrations of alantolactone (0, 1, 2, 4, 6, 8, and 10 μmol/L) for different time points. Cell viability was analyzed with MTT assay. The effect of alantolactone on the apoptosis of K562/ADR cells was measured by flow cytometry. The expression of apoptosis-related proteins after treatment with alantolactone was analyzed using Western blot. RESULTS:
Alantolactone could effectively inhibit the proliferation of K562/ADR cells in dose- and time- dependent manner, the IC50 value of alantolactone treatment of K562/ADR cells for 24 h was 4.7 μmol/L (P<0.05). Flow cytometric analysis displayed that the apoptotic rates were 1.35%, 16.91%, 29.61% and 46.26%, respectively, after treatment with alantolactone at 0, 2.5, 5 and 7.5 μmol/L. Meanwhile, the expression of Bcl-2 and BCR-ABL proteins were significantly decreased and that of Bax, cytochrome C, cleaved-caspase-9, cleaved-caspase-3 and cleaved-PARP increased by alantolactone treatment. CONCLUSION:
Alantolactone had obvious inhibitory effect on the proliferation of K562/ADR cells through the caspase dependent mitochondrial(or intrinsic)apoptotic pathway.
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Authors | Chunhui Yang, Hong Cai, Jiangzhou Yan, Jingbo Yang, Meiyan Sun, Xiuxiang Meng, Tonghui Ma |
Journal | Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
(Zhonghua Xue Ye Xue Za Zhi)
Vol. 35
Issue 6
Pg. 515-8
(Jun 2014)
ISSN: 0253-2727 [Print] China |
PMID | 24985175
(Publication Type: English Abstract, Journal Article)
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Chemical References |
- BAX protein, human
- Lactones
- Proto-Oncogene Proteins c-bcl-2
- Sesquiterpenes, Eudesmane
- bcl-2-Associated X Protein
- Fusion Proteins, bcr-abl
- CASP3 protein, human
- CASP9 protein, human
- Caspase 3
- Caspase 9
- alantolactone
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Topics |
- Apoptosis
- Caspase 3
(metabolism)
- Caspase 9
(metabolism)
- Cell Proliferation
(drug effects)
- Fusion Proteins, bcr-abl
(metabolism)
- Humans
- K562 Cells
- Lactones
(pharmacology)
- Proto-Oncogene Proteins c-bcl-2
(metabolism)
- Sesquiterpenes, Eudesmane
(pharmacology)
- bcl-2-Associated X Protein
(metabolism)
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