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Abstract Title:

[Isoalantolactone Inhibits Proliferation of K562/A02 Cells through Caspase-Dependent Apoptotic Pathway].

Abstract Source:

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2017 Feb ;25(1):110-114. PMID: 28245385

Abstract Author(s):

Yong-Hai Guan, Xiao-Dan Zhang, Hong Cai, Chun-Hui Yang

Article Affiliation:

Yong-Hai Guan

Abstract:

OBJECTIVE: To explore the apoptosis-inducing effects of isoalantolactone on chronic myeloid leukemia drug-resistant cell line K562/A02.

METHODS: K562/A02 cells were treated with 0, 6.25, 12.5, 25, 50, and 100µmol/L isoalantolactone for 12 h, 24 h, and 48 h. The cell viability was analyzed with CCK8 assay. The effects of isoalantolactone on mitochondrial membrane potential (MMP), reactive oxygen species(ROS) and apoptosis of K562/A02 cells were measured by flow cytometry. The apoptosis related proteinswere analyzed by using Western blot after treatment with isoalantolactone.

RESULTS: Isoalantolactone effectively inhibited the proliferation of K562/A02 cells in dose- and time-dependent manner, the ICvalue of isoalantolactone in K562/A02 cells at 24 h was about (15±1.42) µmol/L (P<0.05). Flow cytometric analysis displayed that after treatment of K562/A02 cells with 0, 10, 15, and 20µmol/L of isoalantolactone, apoptotic rate were 1.35±0.52%, 18.07±4.03%, 27.53±3.01%, and 34.99±4.91%, respectively, mitochondrial membrane potential was 96.42±3.59%, 74.25±6.91%, 60.97±5.69%, and 31.28±4.95%, respectively. Otherwise, isoalantolactone induced accumulation of intracellular reactive oxygen species(ROS) in K562/A02 cells (5.03±1.43%, 17.55±3.85%, 32.09±3.23%, and 44.38±5.92%). Meanwhile, isoalantolactone significantly down-regulated the expression of BCL-2 protein and up-regulated the expression of BAX, cytochrome C, cleaved-caspase-9, cleaved-caspase-3, and cleaved-PARP.

CONCLUSION: Isoalantolactone significantly inhibits K562/A02 cell proliferation mainly via caspase-dependent apoptotic pathway.

Study Type : In Vitro Study

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