机构地区:[1]延边大学附属医院口腔科,吉林延吉133000 [2]延边大学医学院病理学教研室,吉林延吉133002 [3]吉林大学中日联谊医院妇产科,吉林长春130033
出 处:《吉林大学学报(医学版)》2020年第6期1182-1186,I0004,共6页Journal of Jilin University:Medicine Edition
基 金:吉林省教育厅“十三五”科学技术项目资助课题(JJKH20200524KJ)。
摘 要:目的:探讨小豆蔻明(CAR)对宫颈癌HeLa细胞增殖的影响,并阐明其可能的作用机制。方法:宫颈癌HeLa细胞分为对照组(不进行任何处理)和不同浓度(10、20和40μmol∙L-1)CAR组(给予10、20和40μmol∙L-1CAR)。CCK-8法检测处理24、48和72 h后各组宫颈癌HeLa细胞活性,菌落形成实验检测各组宫颈癌HeLa细胞克隆形成数,Hoechst33258染色观察各组宫颈癌HeLa细胞凋亡形态表现,Western blotting法检测各组宫颈癌HeLa细胞中B细胞淋巴瘤2(Bcl-2)、Bcl-2相关X蛋白(Bax)、磷酸化磷脂酰肌醇3激酶(p-PI3K)和磷酸化蛋白激酶B(p-AKT)蛋白表达水平。结果:与对照组比较,各时间点不同浓度CAR组HeLa细胞活性明显降低(24 h:P=0.0118;48 h:P=0.0004;72 h:P=0.0022);与对照组比较,不同浓度CAR组HeLa细胞克隆形成数均明显降低(P<0.01);与对照组比较,不同浓度CAR组HeLa细胞出现明显核聚集、皱缩或碎裂的凋亡形态;与对照组比较,不同浓度CAR组HeLa细胞中Bcl-2、p-PI3K(P=0.0118)和p-AKT(P=0.0349)蛋白表达水平明显降低,Bax蛋白表达水平明显升高,Bcl-2/Bax比值明显降低(P<0.01)。结论:CAR通过调控PI3K/AKT信号通路诱导凋亡并抑制HeLa细胞增殖。Objective:To investigate the effect of cardamom(CAR)on the proliferation of the cervical cancer HeLa cells,and to clarify its possible mechanism.Methods:The cervical cancer HeLa cells were divided into control group(given no treatment)and different concentrations(10,20,and 40μmol∙L-1)of CAR groups(given different concerntrations of CAR).CCK-8 method was used to detect the viabilities of the cervical cancer HeLa cells in various groups at 24,48,and 72 h after treatment;the colony formation experiment was used to detect the clone formation number of the cervical cancer HeLa cells in various groups;and the apoptotic morphology of cervical cancer HeLa cells in various groups was observed by Hoechst33258 staining;Western blotting method was used to detect the expression levels of B-cell lymphoma-2(Bcl-2),Bcl-2 associated X protein(Bax),phosphorylated-phosphatidylinositol 3-kinase(p-PI3K),and phosphorylated-protein kinase B(p-AKT)proteins in the HeLa cells in various groups.Results:Compared with control group,the viabilities of the cervical cancer HeLa cells in different concentrations of CAR groups after treated for different time were decreased(24 h:P=0.0118;48 h:P=0.0004;72 h:P=0.0022);compared with control group,the clone formation number of HeLa cells in different concentrations of CAR groups was significantly decreased(P<0.01);compared with control group,the apoptotic morphology of HeLa cells in different concentrations of CAR groups showed as nuclear aggregation,shrinkage or fragmentation;compared with control group,the expression levels of Bcl2,p-PI3K(P=0.0118),and p-AKT(P=0.0349)proteins in the cervical cancer HeLa cells in different concentrations of CAR groups were significantly decresed,while the levels of Bax protein were increased,and the ratios of Bcl-2/Bax were decreased(P<0.01).Conclusion:CAR can induce the apoptosis and inhibit the proliferation of cervical cancer HeLa cells by regulating the PI3K/AKT signaling pathway.
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