国际外科学杂志
國際外科學雜誌
국제외과학잡지
INTERNATIONAL JOURNAL OF SURGERY
2013年
2期
95-98,封3
,共5页
自噬%肝癌细胞%NF-E2相关因子2%细胞周期
自噬%肝癌細胞%NF-E2相關因子2%細胞週期
자서%간암세포%NF-E2상관인자2%세포주기
Autophagy%Hepatoma cells%NF-E2-related factor 2%Cell cycle
目的 探索Nrf2-ARE通路对肝癌HepG2细胞增生与细胞自噬的影响.为临床探索有效的肝癌综合治疗方案提供实验依据.方法 培养肝癌HepG2细胞,用MTr比色法和流式细胞仪检测肝癌HepG2细胞增生抑制率及细胞周期各时相的变化.用倒置相差显微镜和荧光显微镜对肝癌细胞自噬进行定性观察.结果 Nrf2抑制剂BML-111组的肝癌HepG2细胞抑制率明显高于对照组(P＜0.05),对照组的肝癌HepG2细胞抑制率明显高于Nrf2诱导剂EGb组(P＜0.05);流式细胞仪示Nrf2抑制剂BML-111组细胞周期中G1期细胞增多,S期细胞减少,G2/M期细胞相对增多(P ＜0.05);Nrf2诱导剂EGb组细胞周期中G1期细胞减少,S期细胞增多,G2/M期细胞相对减少(P＜0.05).倒置相差显微镜和荧光显微镜检测:Nrf2抑制剂BML-111组肝癌HepG2细胞质中有大小不等的空泡及自噬体形成.结论 Nrf2-ARE通路对肝癌HepG2细胞增生及其自噬有反向抑制作用.抑制Nrf2-ARE通路后肝癌HepG2细胞多停留在细胞周期的G1期.
目的 探索Nrf2-ARE通路對肝癌HepG2細胞增生與細胞自噬的影響.為臨床探索有效的肝癌綜閤治療方案提供實驗依據.方法 培養肝癌HepG2細胞,用MTr比色法和流式細胞儀檢測肝癌HepG2細胞增生抑製率及細胞週期各時相的變化.用倒置相差顯微鏡和熒光顯微鏡對肝癌細胞自噬進行定性觀察.結果 Nrf2抑製劑BML-111組的肝癌HepG2細胞抑製率明顯高于對照組(P＜0.05),對照組的肝癌HepG2細胞抑製率明顯高于Nrf2誘導劑EGb組(P＜0.05);流式細胞儀示Nrf2抑製劑BML-111組細胞週期中G1期細胞增多,S期細胞減少,G2/M期細胞相對增多(P ＜0.05);Nrf2誘導劑EGb組細胞週期中G1期細胞減少,S期細胞增多,G2/M期細胞相對減少(P＜0.05).倒置相差顯微鏡和熒光顯微鏡檢測:Nrf2抑製劑BML-111組肝癌HepG2細胞質中有大小不等的空泡及自噬體形成.結論 Nrf2-ARE通路對肝癌HepG2細胞增生及其自噬有反嚮抑製作用.抑製Nrf2-ARE通路後肝癌HepG2細胞多停留在細胞週期的G1期.
목적 탐색Nrf2-ARE통로대간암HepG2세포증생여세포자서적영향.위림상탐색유효적간암종합치료방안제공실험의거.방법 배양간암HepG2세포,용MTr비색법화류식세포의검측간암HepG2세포증생억제솔급세포주기각시상적변화.용도치상차현미경화형광현미경대간암세포자서진행정성관찰.결과 Nrf2억제제BML-111조적간암HepG2세포억제솔명현고우대조조(P＜0.05),대조조적간암HepG2세포억제솔명현고우Nrf2유도제EGb조(P＜0.05);류식세포의시Nrf2억제제BML-111조세포주기중G1기세포증다,S기세포감소,G2/M기세포상대증다(P ＜0.05);Nrf2유도제EGb조세포주기중G1기세포감소,S기세포증다,G2/M기세포상대감소(P＜0.05).도치상차현미경화형광현미경검측:Nrf2억제제BML-111조간암HepG2세포질중유대소불등적공포급자서체형성.결론 Nrf2-ARE통로대간암HepG2세포증생급기자서유반향억제작용.억제Nrf2-ARE통로후간암HepG2세포다정류재세포주기적G1기.
Objective To explore the influence of HepG2 cells' proliferation and autophagy by the Nrf2-ARE pathway,and provide the experimental basis for clinical exploring effective liver cancer treatment.Methods Hepatic carcinoma HepG2 cells were cultured,and its proliferation inhibition rates and the change of cell cycle' s in each phase were explored by the MTT assay and flow cytometry.The hepatoma cells' autophagy was qualitative observed by inverted phase contrast microscope and fluorescence microscope.Results Inhibitory rate of HepG2 cells was obviously higher in the Nrf2 inhibitor BML-111 group than control group (P ＜ 0.05),and the control group was aslo obviously higher than the Nrf2 inducer EGb group (P ＜ 0.05).Flow cytometric analysis showed that G1 phase cells in the cell cycle increased,S phase cells reduced and G2/M period cells relatively increased in the Nrf2 inhibitor BML-111 group.But G1 phase cells reduced,S phase cells increased and G2/M period cells relative reduced in the Nrf2 inducer EGb group.Inverted phase contrast microscope and fluorescence microscope checked that ranging from the size of the bubble and autophagosome formed in Hepatoma HepG2 cytoplasmic of the Nrf2 inhibitor BML-111 group.Conclusions The Nrf2-ARE pathway played an reverse inhibition on HepG2 cells' proliferation and autophagy.After the inhibition of Nrf2-ARE pathway,HepG2 cells mostly stayed in the G1 phase of the cell cycle.
