Inhibitory effect of alantolactone on the proliferation of K562/ADR cells and its mechanism.

Chunhui Yang; Hong Cai; Jiangzhou Yan; Jingbo Yang; Meiyan Sun; Xiuxiang Meng; Tonghui MA

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Inhibitory effect of alantolactone on the proliferation of K562/ADR cells and its mechanism.

VernacularTitle:土木香内酯对K562/ADR细胞增殖的抑制作用及其机制探讨
Author: Chunhui YANG ¹ ; Hong CAI ¹ ; Jiangzhou YAN ¹ ; Jingbo YANG ¹ ; Meiyan SUN ¹ ; Xiuxiang MENG ¹ ; Tonghui MA ¹
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1. Department of Laboratory Hematology, College of Laboratory Medicine, Dalian Medical University, Dalian 116044, China.
Publication Type:Journal Article
MeSH: 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
From: Chinese Journal of Hematology 2014;35(6):515-518
CountryChina
Language:Chinese
Abstract:
OBJECTIVETo explore the inhibitory effect of alantolactone on the proliferation of adriamycin-resistant human chronic myelogenous leukemia cell line K562/ADR cells and its mechanism.
METHODSK562/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.
RESULTSAlantolactone 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.
CONCLUSIONAlantolactone had obvious inhibitory effect on the proliferation of K562/ADR cells through the caspase dependent mitochondrial(or intrinsic)apoptotic pathway.