Effects of Sinopodophyllum hexundrum on apoptosis in K562 cells.
- Author:
Fang-Zhu ZHOU
1
;
Xin WANG
;
An-Ya DAI
;
Zheng-Lan HUANG
;
Hui LI
;
Ning-Shu HUANG
;
Wen-Li FENG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Caspase 3; metabolism; Cell Proliferation; Drugs, Chinese Herbal; pharmacology; Fusion Proteins, bcr-abl; metabolism; Humans; K562 Cells; Mitochondria; metabolism; STAT5 Transcription Factor; metabolism; Signal Transduction
- From: Journal of Southern Medical University 2016;37(2):226-231
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of Sinopodophyllum hexundrum on apoptosis in K562 cells.
METHODSK562 cells were treated with Sinopodophyllum hexundrum at different concentrations and for different lengths of time to determine the optimal conditions of SinoPodophyllum hexandrum treatment for K562 cells using CCK8 assay. The cell apoptotic rate was detected by flow cytometry, and the cell morphology and nuclear morphology of K562 cells were observed with Wright staining and DPAI staining, respectively. The protein expressions of BCR/ABL, p-BCR/ABL, STAT5, p-STAT5 and the apoptosis-related proteins PARP, caspase-3 and cleaved-caspase-3 were determined with Western blotting.
RESULTSThe cell proliferation was inhibited in a concentration-and time-dependent manner by 1, 2, and 3 µg/mL Sinopodophyllum hexundrum. The treatment was optimal with a Sinopodophyllum hexundrum concentration of 2 µg/mL a treatment time of 48 h, and the cell apoptotic rate increased in a time-dependent manner and significantly increased at 48 h (P<0.001). The expression of apoptosis-related proteins PARP, caspase-3 and cleaved-caspase-3 were also activated in a time-dependent manner. The cells showed typical apoptotic changes after treatment with 2 µg/mL Sinopodophyllum hexundrum for 48 h with significantly reduced expressions of BCR/ABL, p-BCR/ABL, STAT5, AND p-STAT5.
CONCLUSIONSinopodophyllum hexundrum promotes K562 cell apoptosis possibly by inhibiting BCR/ABL-STAT5 survival signal pathways and activating the mitochondrion-associated apoptotic pathways.