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
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篇名: | 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 |
TITLE: | Study on the effect of natural compound XCQ-9 of Cynanchum paniculatum on the proliferation and apoptosis of Jurkat cell and its mechanism |
摘要: | 目的 探讨徐长卿中天然产物XCQ-9抑制人急性T淋巴细胞白血病Jurkat细胞增殖和凋亡的作用及可能机制。方法以Jurkat细胞作为白血病细胞模型,采用MTT法测定0(空白对照)、2.5、5、10、20、40μmol/LXCQ-9作用24、48、72h后对Jurkat细胞增殖的抑制作用。用0(空白对照)、2.5、5、10μmol/LXCQ-9作用于Jurkat细胞24、48h后,利用流式细胞术分析XCQ-9对细胞周期和细胞凋亡的影响,并通过Westernblot实验检测上述药物作用24h后细胞中胱天蛋白酶9(Caspase-9)、活化的Caspase-9(CleavedCaspase-9)、Caspase-3、活化的Caspase-3(CleavedCaspase-3)、聚腺苷二磷酸-核糖聚合酶(PARP)、活化的PARP(CleavedPARP)、细胞周期蛋白依赖性激酶1(CDK1)和细胞周期蛋白B1(CyclinB1)的表达情况。结果与空白对照比较,不同浓度XCQ-9均可显著降低Jurkat细胞的存活率(P<0.01),并呈时间和浓度依赖性趋势。5、10μmol/LXCQ-9作用48h后均可显著诱导Jurkat细胞凋亡(P<0.05或P<0.01),将细胞周期阻滞在G2期(P<0.01)。10μmol/LXCQ-9作用24h后,可显著下调细胞中CDK1、Caspase-9蛋白的表达(P<0.01),上调细胞中CyclinB1、CleavedCaspase-9、CleavedCaspase-3和CleavedPARP蛋白的表达(P<0.05或P<0.01)。结论XCQ-9通过诱导G2期阻滞抑制Jurkat细胞增殖,并激活Caspase通路促进细胞凋亡,从而发挥其抗肿瘤作用。 |
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. |
期刊: | 2023年第34卷第01期 |
作者: | 韦学耐;杨坤;刘琴;赵鹏;晏英;李艳梅 |
AUTHORS: | WEI Xuenai,YANG Kun,LIU Qin,ZHAO Peng,YAN Ying,LI Yanmei |
关键字: | XCQ-9;徐长卿;人急性T淋巴细胞白血病;Jurkat细胞;细胞凋亡;细胞周期;胱天蛋白酶途径 |
KEYWORDS: | XCQ-9; Cynanchum paniculatum; human T- |
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