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没食子酸表没食子儿茶素酯通过 ROS 介导的 AKT/JNK 和 p53 信号通路诱导 HepG2 细胞凋亡。

Epigallocatechin-3-gallate Induced HepG2 Cells Apoptosis through ROSmediated AKT /JNK and p53 Signaling Pathway.

机构信息

Department of Obstetrics and Gynecology, Ningbo First Hospital, Ningbo Hospital of Zhejiang University, Ningbo, Zhejiang, China.

Center Laboratory, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.

出版信息

Curr Cancer Drug Targets. 2023;23(6):447-460. doi: 10.2174/1568009622666220705101642.

DOI:10.2174/1568009622666220705101642

PMID:35792125

Abstract

BACKGROUND

Hepatocarcinoma is the third leading cause of cancer-related deaths around the world. Recently, some studies have reported that Epigallocatechin-3-gallate (EGCG) may have the anti-cancer potential. However, the affection and putative mechanisms of cytotoxicity induced by EGCG in HepG2 cells remain unknown. Based on the above, the present study evaluated the effect of EGCG on the cytotoxic and anti-cancer mechanisms of HepG2 cells.

METHODS

The effect of EGCG on the apoptosis of Hep-G2 cells and its mechanism were studied by cell counting kit-8, mitochondrial membrane potential assay with JC-1, Annexin V-FITC apoptosis detection, cell cycle, and apoptosis analysis, one step TUNEL apoptosis assay, caspase 3 activity assay, caspase 9 activity Assay, Reactive Oxygen Species assay, and Western blot.

RESULTS

EGCG-induced HepG2 cell apoptosis was confirmed by accumulation of the sub-G1 cells population, translocation of phosphatidylserine, depletion of mitochondrial membrane potential, DNA fragmentation, caspase-3 activation, caspase-9 activation, and poly (ADP-ribose) polymerase cleavage. Furthermore, EGCG enhanced cytotoxic effects on HepG2 cells and triggered intracellular reactive oxygen species; the signaling pathways of AKT, JNK, and p53 were activated to advance cell apoptosis.

CONCLUSION

The results reveal that EGCG may provide useful information on EGCG-induced HepG2 cell apoptosis and be an appropriate candidate for cancer chemotherapy.

摘要

背景

肝癌是全球癌症相关死亡的第三大主要原因。最近，一些研究报告称，表没食子儿茶素没食子酸酯（EGCG）可能具有抗癌潜力。然而，EGCG 在 HepG2 细胞中诱导细胞毒性的作用和潜在机制尚不清楚。基于上述情况，本研究评估了 EGCG 对 HepG2 细胞细胞毒性和抗癌机制的影响。

方法

通过细胞计数试剂盒-8、JC-1 线粒体膜电位测定、Annexin V-FITC 凋亡检测、细胞周期和凋亡分析、一步 TUNEL 凋亡检测、caspase 3 活性测定、caspase 9 活性测定、活性氧测定和 Western blot 研究 EGCG 对 Hep-G2 细胞凋亡的影响及其机制。

结果

通过亚 G1 细胞群的积累、磷脂酰丝氨酸易位、线粒体膜电位耗竭、DNA 片段化、caspase-3 激活、caspase-9 激活和聚（ADP-核糖）聚合酶切割证实 EGCG 诱导 HepG2 细胞凋亡。此外，EGCG 增强了对 HepG2 细胞的细胞毒性作用，并引发细胞内活性氧；AKT、JNK 和 p53 信号通路被激活以促进细胞凋亡。