Gambogic acid induces apoptosis of Jurkat cell through the MAPK signal pathway / 中国实验血液学杂志
Journal of Experimental Hematology
; (6): 587-591, 2012.
Article
in Zh
| WPRIM
| ID: wpr-263344
Responsible library:
WPRO
ABSTRACT
The aim of this study was to investigate the apoptosis-inducing effect of gambogic acid (GA) on Jurkat cells and its underlying signaling pathway. Apoptosis induced by GA and some inhibitors was assayed by Annexin V/PI doubling staining. The levels of caspase 3, caspase 8 and caspase 9 activated in living Jurkat cells were measured by flow cytometry. The expressions of caspase 3, caspase 9, p-JNK and P38 were detected by Western blot. The results showed that GA induced apoptosis of Jurkat cells in a dose-dependent manner. The positive cell number of activated caspase 3, caspase 8, caspase 9 and the levels of activated caspase 3, caspase 9, p-JNK, P38 increased after Jurkat cells were treated with GA. ROS, CaMKII, caspase 3, caspase 9, MAPKK, JNK1/2 and P38 inhibitors had some significant effect on GA-induced apoptosis. ROS, CaMKII, MAPKK, JNK1/2 and P38 inhibitors decreased the levels of activated caspase 3, caspase 9 by GA.ROS, CaMKII, MAPKK, JNK1/2 inhibitors decreased the levels of p-JNK by GA. ROS, CaMKII, MAPKK, P38 inhibitors decreased the levels of P38 by GA. It is concluded that GA induced apoptosis of Jurkat cells by activated caspases through activating of ROS-CaMKII-MAPKK-JNK/P38 pathway.
Full text:
1
Index:
WPRIM
Main subject:
Pharmacology
/
Apoptosis
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Jurkat Cells
/
MAP Kinase Signaling System
/
Xanthones
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JNK Mitogen-Activated Protein Kinases
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P38 Mitogen-Activated Protein Kinases
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Caspase 3
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Caspase 9
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Metabolism
Limits:
Humans
Language:
Zh
Journal:
Journal of Experimental Hematology
Year:
2012
Type:
Article