5-HT再摄取抑制剂氟西汀诱导HepG2细胞凋亡

目的通过观察5-HT再摄取特异性抑制剂氟西汀对人肝癌细胞系HepG2细胞凋亡的影响,探索氟西汀治疗肝细胞癌的可能性。方法采用不同浓度氟西汀(5μmol、7.5μmol、10μmol、12.5μmol、15μmol)分别处理HepG2细胞24 h、48 h,AnnexinV-FITC/PI流式细胞术和蛋白水解酶3免疫荧光法检测细胞凋亡。结果 10μmol、12.5μmol氟西汀处理24 h早期凋亡率分为(14.41±5.40)%、(19.43±5.91)%,与对照组(4.05±1.90)%相比差异均具有统计学意义(均P0.05),5μmol氟西汀处理48 h早期凋亡率为(20.32±6.23)%,与对照组(12.40±4.18)%相比差异有统计学意义(P0.05),10μmol及12.5μmol氟西汀处理24 h活化caspase 3阳性细胞显著增加。结论氟西汀具有促进HepG2细胞凋亡的作用,为临床上应用氟西汀治疗肝细胞癌患者提供了依据。

5-HT reuptake specific inhibitor fluoxetine induce HepG2 apoptosis

Objective To investigate the effect of 5-hydroxytryptamine (5-HT) reuptake specific inhibitor fluoxetine on apoptosis of human hepatocellular carcinoma cell line (HepG2).Methods HepG2 cells were treated with different concentrations of fluoxetine (5 μM,7.5 μM,10 μM,12.5 μM,15 μM) for 24 h and 48 h,respectively.Apoptosis was detected using Annexin V-FITC/PI flow cytometry and proteolytic enzyme 3 immunofluorescence assay.Results The 24 h apoptosis rates of HepG2 treated with 10μM and 12.5 μM fluoxetine were 14.41 ％ ± 5.40％ and 19.43％ ± 5.91 ％,which were significantly higher than that with control treatment (4.05％ ± 1.90％,both P＜0.05),respectively.The apoptosis rate was 20.32％ ± 6.23％ after 48 h treatment with 5μM fluoxetine,which was significantly higher than that with control treatment (12.40％± 4.18％,P＜0.05).Treatment with 10 μM or 12.5 μM fluoxetine for 24 h significantly increased activated caspase 3 positive cells.Conclusion Fluoxetine could promote the apoptosis of HepG2 cells in a dose-dependent manner,which provides a clue for the clinical application of fluoxetine in the treatment of patients with hepatocellular carcinoma.