Reactive oxygen species generation and mitochondrial dysfunction for the initiation of apoptotic cell death in human hepatocellular carcinoma HepG2 cells by a cyclic dipeptide Cyclo(-Pro-Tyr)

2020 ◽  
Vol 47 (5) ◽  
pp. 3347-3359
Author(s):  
Gayathri Karanam ◽  
Madan Kumar Arumugam
Keyword(s):  
Hepatocellular Carcinoma ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Mitochondrial Dysfunction ◽  
Hepg2 Cells ◽  
Apoptotic Cell ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cyclic Dipeptide

scholarly journals Rosmarinic acid induces programmed cell death in Arabidopsis seedlings through reactive oxygen species and mitochondrial dysfunction

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0208802 ◽  
Author(s):  
Fabrizio Araniti ◽  
Aitana Costas-Gil ◽  
Luz Cabeiras-Freijanes ◽  
Antonio Lupini ◽  
Francesco Sunseri ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Mitochondrial Dysfunction ◽  
Rosmarinic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Ivalin Induces Mitochondria-Mediated Apoptosis Associated with the NF-κB Activation in Human Hepatocellular Carcinoma SMMC-7721 Cells

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3809
Author(s):  
Zhuo Han ◽  
Fang-yuan Liu ◽  
Shi-qi Lin ◽  
Cai-yun Zhang ◽  
Jia-hui Ma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Mitochondrial Pathway ◽  
Human Hepatocellular Carcinoma ◽  
Induction Effect ◽  
Oxygen Species ◽  
Microtubule Depolymerization ◽  
Apoptotic Effect

Ivalin, a natural compound isolated from Carpesium divaricatum, showed excellent microtubule depolymerization activities among human hepatocellular carcinoma in our previous work. Here, we investigated its functions on mitochondria-mediated apoptosis in hepatocellular carcinoma SMMC-7721 cells. DAPI (4′,6-diamidino-2-phenylindole) staining, annexin V-fluorexcein isothiocyanate (FITC) apoptosis detection, and western blotting were applied to explore the apoptotic effect of Ivalin. Next, the induction effect of Ivalin on the mitochondrial pathway was also confirmed via a series of phenomena including the damage of mitochondria membrane potential, mitochondria cytochrome c escape, cleaved caspase-3 induction, and the reactive oxygen species generation. In this connection, we understood that Ivalin induced apoptosis through the mitochondrial pathway and the overload of reactive oxygen species. Furthermore, we found that the activation of nuclear factor-κB (NF-κB) and subsequent p53 induction were associated with the apoptotic effect of Ivalin. These data confirmed that Ivalin might be a promising pro-apoptotic compound that can be utilized as a potential drug for clinical treatment.

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