Study on the effect of natural compound XCQ-9 of Cynanchum paniculatum on the proliferation and apoptosis of Jurkat cell and its mechanism
- VernacularTitle:徐长卿中的天然产物XCQ-9对Jurkat细胞增殖和凋亡的影响及机制研究
- Author:
Xuenai WEI
1
;
Kun YANG
1
;
Qin LIU
1
;
Peng ZHAO
1
;
Ying YAN
2
;
Yanmei LI
3
Author Information
1. School of Pharmaceutical，Guizhou Medical University，Guiyang 550025，China;Key Laboratory of Chemistry for Natural Products，Guizhou Province and Chinese Academy of Sciences，Guiyang 550014，China
2. School of Medicine and Health Management，Guizhou Medical University，Guiyang 550025，China
3. School of Pharmaceutical，Guizhou Medical University，Guiyang 550025，China
- Publication Type:Journal Article
- Keywords:
XCQ-9;
Cynanchum paniculatum;
human T-
- From:
China Pharmacy
2023;34(1):47-51
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the inhibitory effect of natural compound XCQ-9 of Cynanchum paniculatum on the proliferation and apoptosis of Jurkat cell line of human T-cell acute lymphoblastic leukemia and its possible mechanism. METHODS Jurkat cell was used as the leukemia cell model， and MTT assay was adopted to detect the inhibitory effects of 0 （blank control）， 2.5， 5， 10， 20 and 40 μmol/L XCQ-9 on the proliferation of Jurkat cell after treated for 24， 48， 72 h. After treated with 0 （blank control）， 2.5， 5， 10 μmol/L XCQ-9 for 24 h and 48 h， the cell cycle and apoptosis were analyzed by flow cytometry. The expressions of Caspase-9， Cleaved Caspase-9， Caspase-3， Cleaved Caspase-3， poly ADP-ribose poly-merase （PARP）， Cleaved-PARP， cyclin-dependent kinase 1 （CDK1） and Cyclin B1 were detected by Western blot after treated for 24 h. RESULTS Compared with blank control group， XCQ-9 at different concentrations could significantly decrease the survival rate of Jurkat cells （P＜0.01）， and showed a dose and time-dependent manner. After 48 h treatment of 5， 10 μmol/L XCQ-9， Jurkat cell apoptosis was induced significantly （P＜0.05 or P＜0.01）， and the cell was arrested in G2 phase （P＜0.01）. After 24 h treatment of 10 μmol/L XCQ-9， the protein expressions of CDK1 and Caspase-9 were remarkably down-regulated （P＜0.01）， while the protein expressions of Cyclin B1， Cleaved Caspase-9， Cleaved Caspase-3 and Cleaved PARP were significantly up-regulated （P＜0.05 or P＜0.01）. CONCLUSIONS XCQ-9 plays anti-tumor effect through inducing G2 phase arrest to inhibit proliferation and 5008） activating Caspase pathway to increase apoptosis.
