CAJ | 학술논문

目的观察柯里拉京对人肺腺癌细胞株A549的杀伤作用.方法通过体外细胞培养、噻唑蓝(MTT)比色法、Western blot、流式细胞仪观察35 μmol/L柯里拉京对人肺腺癌细胞A549的增殖、细胞周期、细胞凋亡和Notch信号通路蛋白的影响.结果 35 μmol/L柯里拉京能够抑制人肺腺癌细胞A549的增殖;20 μmol/L柯里拉京诱导细胞早期凋亡从2.0％上升到5.4％,晚期凋亡从3.1％上升至12.8％,40 μmol/L可见早期凋亡上升到7.0％,晚期凋亡上升至13.7％;35 μmol/L柯里拉京处理后可抑制人肺腺癌细胞株A549中Notch1、NICD和哺乳动物雷帕霉素靶蛋白(mTOR)蛋白的表达.结论柯里拉京能够抑制人肺腺癌细胞A549细胞的增殖并诱导其凋亡,可能是通过Notch信号通路发挥作用.
목적 관찰가리랍경대인폐선암세포주A549적살상작용.방법 통과체외세포배양、새서람(MTT)비색법、Western blot、류식세포의관찰35 μmol/L가리랍경대인폐선암세포A549적증식、세포주기、세포조망화Notch신호통로단백적영향.결과 35 μmol/L가리랍경능구억제인폐선암세포A549적증식;20 μmol/L가리랍경유도세포조기조망종2.0％상승도5.4％,만기조망종3.1％상승지12.8％,40 μmol/L가견조기조망상승도7.0％,만기조망상승지13.7％;35 μmol/L가리랍경처리후가억제인폐선암세포주A549중Notch1、NICD화포유동물뢰파매소파단백(mTOR)단백적표체.결론 가리랍경능구억제인폐선암세포A549세포적증식병유도기조망,가능시통과Notch신호통로발휘작용.
Objective To study the killing effects of corilagin on human lung adenocarcinoma cell line A549.Methods Cell culture,methyl thiazol tetrazolium (MTT) assay,Western blotting and flow cytometry were used to detect the cell cycle,apoptosis,Notch signaling pathway proteins of human lung adenocarcinoma cell line A549 treated with corilagin.Results 35 μmol/L corilagin could inhibit the proliferation of human lung adenocarcinoma cell line A549.20 μmol/L corilagin increased early apoptosis from 2.0％ to 5.4％,and late apoptosis from 3.1％ to 12.8％.40 μmol/L corilagin increased early apoptosis to 7.0％ and late apoptosis to 13.7％.Corilagin could inhibit the expression of Notch1,NICD and mammalian target of rapamycin (mTOR) protein in A549 cells.Conclusion Corilagin could inhibit the proliferation of human lung adenocarcinoma cell line A549 and induce apoptosis possibly through the Notch signaling pathway.