柚皮苷通过阻断JAK/STAT信号通路抑制Eca109人食管癌细胞的增殖、侵袭并促进其凋亡  

Naringin inhibits the proliferation and invasion of Eca109 esophageal cancer cells and promotes its apoptosis by blocking JAK/STAT signal pathway

作　　者：杨锋 姜涛 张利宏[2] 齐亚刚 杨占祥[2] YANG Feng;JIANG Tao;ZHANG Lihong;QI Yagang;YANG Zhanxiang(Department of Thoracic Surgery,Tangdu Hospital,Xi'an 710038;Department of Hepatobiliary Surgery,Baoji Central Hospital,Baoji 721001,China)

机构地区：[1]空军军医大学唐都医院胸外科,陕西西安710038 [2]宝鸡市中医医院肝胆外科,陕西宝鸡721001

出　　处：《细胞与分子免疫学杂志》2021年第12期1085-1091,共7页Chinese Journal of Cellular and Molecular Immunology

基　　金：陕西省自然科学基金(2009 JM4003-4)。

摘　　要：目的探究柚皮苷(NAR)对Eca109食管癌细胞的增殖活性的抑制作用和凋亡的促进作用及其作用机制。方法培养Eca109细胞,采用(0、15、30、45)μmol/LNAR处理24、48、72 h。采用细胞集落形成试验评估Eca109食管癌细胞的集落形成能力,噻唑蓝(MTT)法检测细胞增殖活性,Transwell^(TM)实验检测癌细胞侵袭能力;采用异硫氰酸荧光素标记的膜联素Ⅴ/碘化丙啶(annexinⅤ-FITC/PI)染色检测细胞凋亡,Western blot法检测B细胞淋巴瘤因子2(Bcl2)、Bcl2相关X蛋白(BAX)、细胞色素C(CytC)、胱天蛋白酶3(caspase-3)、caspase-9、Janus激酶2(JAK2)、磷酸化的JAK2(p-JAK2)、信号转导子与转录激活子3(STAT3)、磷酸化的STAT3(p-STAT3)、蛋白激酶B(AKT)、磷酸化的AKT(p-AKT)蛋白表达。结果柚皮苷抑制Eca109细胞增殖活性和细胞集落形成,抑制Eca109细胞的侵袭并促进Eca109细胞凋亡;柚皮苷能够促进BAX、CytC、caspase-3、caspase-9、p-STAT3、p-AKT、AKT和p-JAK2表达,抑制Bcl2表达。结论柚皮苷能通过阻断JAK/STAT信号通路活化抑制Eca109细胞的增殖、侵袭和细胞集落形成并促进其凋亡。Objective To investigate the inhibitory effect of naringin(NAR)on proliferation and apoptosis of Eca109 esophageal cancer cells and its mechanism.Methods Eca109 cells were cultured with 0,15,30,45μmol/L NAR treatment for 24,48 and 72 hours.The colony forming ability of Eca109 esophageal cancer cells was evaluated by cell colony forming assay,the cell proliferation activity was detected by MTT assay,and the invasion ability of cancer cells was detect by Transwell^(TM) assay;Apoptosis was detected by annexinⅤ-FITC/PI double labeling combined with flow cytometry.Western blot analysis was used to detect the protein expression of B-cell lymphoma factor 2(Bcl2),Bcl2 related X protein(BAX),cytochrome C(CytC),caspase-3,caspase-9,Janus kinase 2(JAK2),phosphorylated JAK2(p-JAK2)and signal transducer and activator of transcription 3(STAT3),phosphorylated STAT3(p-STAT3),protein kinase B(AKT),phosphorylated AKT(p-AKT).Results NAR inhibited the proliferation and colony formation of Eca109 cells,suppressed the invasion of Eca109 cells and promoted the apoptosis of Eca109 cells;NAR promoted the expression of BAX,CytC,caspase-3,caspase-9,p-STAT3,p-AKT,AKT and p-JAK2 and inhibited the expression of Bcl2.Conclusion NAR can inhibit the proliferation,invasion,and colony formation of Eca109 cells and promote its apoptosis by blocking the activation of JAK/STAT signal pathway.

关 键 词：食管癌 ECA109细胞 Janus激酶2(JAK2) 信号转导子与转录激活子3(STAT3) 细胞增殖 细胞凋亡 

分 类 号：R285.5[医药卫生—中药学] Q279[医药卫生—中医学]