scholarly journals Mechanistic Insights into Oxidative Stress and Apoptosis Mediated by Tannic Acid in Human Liver Hepatocellular Carcinoma Cells

2019 ◽  
Vol 20 (24) ◽  
pp. 6145 ◽  
Author(s):  
Priscilla Mhlanga ◽  
Pearl O. Perumal ◽  
Anou M. Somboro ◽  
Daniel G. Amoako ◽  
Hezekiel M. Khumalo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Dna Fragmentation ◽  
Tannic Acid ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Dna Integrity ◽  
Liver Hepatocellular Carcinoma ◽  
And Oxidative Stress

The study investigated the cytotoxic effect of a natural polyphenolic compound Tannic acid (TA) on human liver hepatocellular carcinoma (HepG2) cells and elucidated the possible mechanisms that lead to apoptosis and oxidative stress HepG2 cell. The HepG2 cells were treated with TA for 24 h and various assays were conducted to determine whether TA could induce cell death and oxidative stress. The cell viability assay was used to determine the half maximal inhibitory concentration (IC50), caspase activity and cellular ATP were determined by luminometry. Microscopy was employed to determine deoxyribonucleic acid (DNA) integrity, while thiobarbituric acid (TBARS) and nitric oxide synthase (NOS) assays were used to elucidate cellular reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively. Western blotting was used to confirm protein expression. The results revealed that tannic acid induced caspase activation and increased the presence of cellular ROS and RNS, while downregulating antioxidant expression. Tannic acid also showed increased cell death and increased DNA fragmentation. In conclusion, TA was able to induce apoptosis by DNA fragmentation via caspase-dependent and caspase-independent mechanism. It was also able to induce oxidative stress, consequently contributing to cell death.

Effects of Amaranthus cruentus L. on aflatoxin B1- and oxidative stress-induced DNA damage in human liver (HepG2) cells

2018 ◽  
Vol 26 ◽  
pp. 42-48 ◽  
Author(s):  
Grace A. Odongo ◽  
Nina Schlotz ◽  
Susanne Baldermann ◽  
Susanne Neugart ◽  
Benard Ngwene ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Aflatoxin B1 ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Amaranthus Cruentus ◽  
And Oxidative Stress

scholarly journals Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe3O4-RGO Nanocomposites in Human Liver HepG2 cells

Materials ◽  
2020 ◽  
Vol 13 (3) ◽  
pp. 660 ◽  
Author(s):  
Maqusood Ahamed ◽  
Mohd Javed Akhtar ◽  
M. A. Majeed Khan
Keyword(s):  
Oxidative Stress ◽  
Electron Microscopy ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Molecular Level ◽  
Biological Response ◽  
Cycle Arrest ◽  
Transmission Electron ◽  
Mitochondrial Membrane Potential Loss ◽  
And Oxidative Stress

Iron oxide–reduced graphene oxide (Fe3O4-RGO) nanocomposites have attracted enormous interest in the biomedical field. However, studies on biological response of Fe3O4-RGO nanocomposites at the cellular and molecular level are scarce. This study was designed to synthesize, characterize, and explore the cytotoxicity of Fe3O4-RGO nanocomposites in human liver (HepG2) cells. Potential mechanisms of cytotoxicity of Fe3O4-RGO nanocomposites were further explored through oxidative stress. Prepared samples were characterized by UV-visible spectrophotometer, X-ray diffraction, scanning electron microscopy, transmission electron microscopy, and energy dispersive spectroscopy. The results demonstrated that RGO induce dose-dependent cytotoxicity in HepG2 cells. However, Fe3O4-RGO nanocomposites were not toxic. We further noted that RGO induce apoptosis in HepG2 cells, as evidenced by mitochondrial membrane potential loss, higher caspase-3 enzyme activity, and cell cycle arrest. On the other hand, Fe3O4-RGO nanocomposites did not alter these apoptotic parameters. Moreover, we observed that RGO increases intracellular reactive oxygen species and hydrogen peroxide while decrease antioxidant glutathione. Again, Fe3O4-RGO nanocomposites did not exert oxidative stress. Altogether, we found that RGO significantly induced cytotoxicity, apoptosis and oxidative stress. However, Fe3O4-RGO nanocomposites showed good biocompatibility to HepG2 cells. This study warrants further research to investigate the biological response of Fe3O4-RGO nanocomposites at the gene and molecular level.

scholarly journals Loss of protein targeting to glycogen sensitizes human hepatocellular carcinoma cells towards glucose deprivation mediated oxidative stress and cell death

2015 ◽  
Vol 35 (3) ◽  
Author(s):  
Rongqiang Yang ◽  
Mei Zhang ◽  
Amber Renee Gustafson ◽  
Eugenia Wang ◽  
Marsha Paulette Cole ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Protein Targeting ◽  
Glucose Deprivation ◽  
Carcinoma Cells ◽  
Glycogen Accumulation ◽  
Liver Cancer Cells ◽  
Human Hepatocellular Carcinoma Cells ◽  
And Oxidative Stress

PTG is a protein that is critical for glycogen accumulation in various tissues such as the liver. Our present study shows that its loss sensitizes liver cancer cells towards metabolic and oxidative stress.

scholarly journals Nomad Jellyfish Rhopilema nomadica Venom Induces Apoptotic Cell Death and Cell Cycle Arrest in Human Hepatocellular Carcinoma HepG2 Cells

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5185
Author(s):  
Mohamed M. Tawfik ◽  
Nourhan Eissa ◽  
Fayez Althobaiti ◽  
Eman Fayad ◽  
Ali H. Abu Almaaty
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Dna Fragmentation ◽  
Hepg2 Cells ◽  
Apoptotic Cell ◽  
Cycle Arrest ◽  
Jellyfish Venom

Jellyfish venom is a rich source of bioactive proteins and peptides with various biological activities including antioxidant, antimicrobial and antitumor effects. However, the anti-proliferative activity of the crude extract of Rhopilema nomadica jellyfish venom has not been examined yet. The present study aimed at the investigation of the in vitro effect of R. nomadica venom on liver cancer cells (HepG2), breast cancer cells (MDA-MB231), human normal fibroblast (HFB4), and human normal lung cells (WI-38) proliferation by using MTT assay. The apoptotic cell death in HepG2 cells was investigated using Annexin V-FITC/PI double staining-based flow cytometry analysis, western blot analysis, and DNA fragmentation assays. R. nomadica venom displayed significant dose-dependent cytotoxicity on HepG2 cells after 48 h of treatment with IC50 value of 50 μg/mL and higher toxicity (3:5-fold change) against MDA-MB231, HFB4, and WI-38 cells. R. nomadica venom showed a prominent increase of apoptosis as revealed by cell cycle arrest at G2/M phase, upregulation of p53, BAX, and caspase-3 proteins, and the down-regulation of anti-apoptotic Bcl-2 protein and DNA fragmentation. These findings suggest that R. nomadica venom induces apoptosis in hepatocellular carcinoma cells. To the best of the authors’ knowledge, this is the first scientific evidence demonstrating the induction of apoptosis and cell cycle arrest of R. nomadica jellyfish venom.

scholarly journals Sinensetin Induces Autophagic Cell Death through p53-Related AMPK/mTOR Signaling in Hepatocellular Carcinoma HepG2 Cells

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2462
Author(s):  
Seong Min Kim ◽  
Sang Eun Ha ◽  
Ho Jeong Lee ◽  
Shailima Rampogu ◽  
Preethi Vetrivel ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Cell Line ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Apoptotic Cell ◽  
Docking Simulation ◽  
Mtor Signaling ◽  
Autophagic Cell Death ◽  
Anti Cancer

Sinensetin (SIN) has been reported to exhibit anti-inflammatory and anti-cancer activity. However, the cellular and molecular mechanism by which SIN promotes hepatocellular carcinoma (HCC) cell death remains unclear. In the present study, we investigated the induction of cell death by SIN and its underlying mechanism in HepG2 cells, an HCC cell line. We found that SIN significantly induced cell death in HepG2 cells, whereas the proliferation rate of Thle2, human liver epithelial cells, was unaffected by SIN. SIN-treated HepG2 cells were not affected by apoptotic cell death; instead, autophagic cell death was induced through the p53-mediated AMPK/mTOR signaling pathway. Inhibition of p53 degradation led to both autophagy and apoptosis in HepG2 cells. p53 translocation led to SIN-induced autophagy, whereas p53 translocation inhibited SIN-induced apoptosis. However, SIN showed apoptosis in the p53-mutant Hep3B cell line. Molecular docking simulation of the p53 core domain showed effective binding with SIN, which was found significant compared with the known p53 activator, RITA. Collectively, these data suggest that SIN may be a potential anti-cancer agent targeting autophagic cell death in human liver cancer.

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