Toxicogenomic responses of human liver HepG2 cells to silver nanoparticles

Introduction: Obesity is a disorder with low-grade chronic inflammation that plays a key role in the hepatic inflammation and steatosis. Moreover, there are studies to support the role of exosomes in the cellular communications, the regulation of metabolic homeostasis and immunomodulatory activity. Accordingly, we aimed to evaluate the influence of plasma circulating exosomes derived from females with normal-weight and obesity on the secretion of inflammatory cytokines in human liver cells. Methods: Plasma circulating exosomes were isolated from four normal (N-Exo) and four obese (O-Exo) women. The exosomes were characterized and approved for CD63 expression (common exosomal protein marker) and morphology/size using the western blot and TEM methods, respectively. The exosomes were used for stimulation of HepG2 cells in vitro. After 24 h incubation, the protein levels of TNF-α,IL-6, and IL-1β were measured in the culture supernatant of HepG2 cells using the ELISA kit. Results: The protein levels of IL-6 and TNF-α in the cells treated with O-Exo and N-Exo reduced significantly in comparison with control group (P=0.039 and P<0.001 respectively), while significance differences were not found between normal and obese groups (P=0.808, and P=0.978 respectively). However, no significant differences were found between three groups in term of IL-1β levels (P=0.069). Based on the correlation analysis, the protein levels of IL-6 were positively correlated with TNF-α (r 0.978, P<0.001). Conclusion: These findings suggest that plasma circulating exosomes have probably anti-inflammatory properties independently from body mass index and may decrease the secretion of inflammatory cytokines in liver. However, further investigations in vitro and in vivo are needed to address the anti-inflammatory function of N-Exo and O-Exo in human liver cells and/or other cells.

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Assessment of Chemopreventive Potential of the Plant Extracts against Liver Cancer Using Hepg2 Cell Line

Molecules ◽

10.3390/molecules26154593 ◽

2021 ◽

Vol 26 (15) ◽

pp. 4593

Author(s):

Deepthi Venkatachalapathy ◽

Chandan Shivamallu ◽

Shashanka Prasad ◽

Gopenath Thangaraj Saradha ◽

Parthiban Rudrapathy ◽

...

Keyword(s):

Liver Cancer ◽

Vitis Vinifera ◽

Bioactive Compounds ◽

Camellia Sinensis ◽

Hepg2 Cells ◽

Human Liver ◽

Withania Somnifera ◽

Antioxidant Properties ◽

Annexin V ◽

Human Liver Cancer

The edible parts of the plants Camellia sinensis, Vitis vinifera and Withania somnifera were extensively used in ancient practices such as Ayurveda, owing to their potent biomedical significance. They are very rich in secondary metabolites such as polyphenols, which are very good antioxidants and exhibit anti-carcinogenic properties. This study aims to evaluate the anti-cancerous properties of these plant crude extracts on human liver cancer HepG2 cells. The leaves of Camellia sinensis, Withania somnifera and the seeds of Vitis vinifera were collected and methanolic extracts were prepared. Then, these extracts were subjected to DPPH, α- amylase assays to determine the antioxidant properties. A MTT assay was performed to investigate the viability of the extracts of HepG2 cells, and the mode of cell death was detected by Ao/EtBr staining and flow cytometry with PI Annexin- V FITC dual staining. Then, the protein expression of BAX and BCl2 was studied using fluorescent dye to determine the regulation of the BAX and BCl2 genes. We observed that all the three extracts showed the presence of bioactive compounds such as polyphenols or phytochemicals. The W. somnifera bioactive compounds were found to have the highest anti-proliferative activity on human liver cancer cells.

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Oxidative Stress and Apoptotic Responses Elicited by Nostoc-Synthesized Silver Nanoparticles against Different Cancer Cell Lines

Cancers ◽

10.3390/cancers12082099 ◽

2020 ◽

Vol 12 (8) ◽

pp. 2099 ◽

Cited By ~ 3

Author(s):

Reham Samir Hamida ◽

Gadah Albasher ◽

Mashael Mohammed Bin-Meferij

Keyword(s):

Oxidative Stress ◽

Silver Nanoparticles ◽

Cancer Cells ◽

Hepg2 Cells ◽

Caspase 3 ◽

Mammalian Target Of Rapamycin ◽

B Cell Lymphoma ◽

Phosphorylated Akt ◽

Hct 116 ◽

Mcf 7

Green nanoparticles represent a revolution in bionanotechnology, providing opportunities to fight life-threatening diseases, such as cancer, with less risk to the environment and to human health. Here, for the first time, we systematically investigated the anticancer activity and possible mechanism of novel silver nanoparticles (N-SNPs) synthesized by Nostoc Bahar M against the MCF-7 breast cancer cells, HCT-116 colorectal adenocarcinoma cells, and HepG2 liver cancer cells, using cell viability assays, morphological characterization with inverted light and transmission electron microscopy, antioxidants and enzymes (glutathione peroxidase (GPx), glutathione (GSH), adenosine triphosphatase (ATPase), and lactate dehydrogenase (LDH)), and western blotting (protein kinase B (Akt), phosphorylated-Akt (p-Akt), mammalian target of rapamycin (mTOR), B-cell lymphoma 2 (Bcl-2), tumor suppressor (p53), and caspase 3). N-SNPs decreased the viability of MCF-7, HCT-116, and HepG2 cells, with half-maximal inhibitory concentrations of 54, 56, and 80 µg/mL, respectively. They also significantly increased LDH leakage, enhanced oxidative stress via effects on antioxidative markers, and caused metabolic stress by significantly decreasing ATPase levels. N-SNPs caused extensive ultrastructural alterations in cell and nuclear structures, as well as in various organelles. Furthermore, N-SNPs triggered apoptosis via the activation of caspase 3 and p53, and suppressed the mTOR signaling pathway via downregulating apoptosis-evading proteins in MCF-7, HCT-116, and HepG2 cells. Ultrastructural analysis, together with biochemical and molecular analyses, revealed that N-SNPs enhanced apoptosis via the induction of oxidative stress and/or through direct interactions with cellular structures in all tested cells. The cytotoxicity of Nostoc-mediated SNPs represents a new strategy for cancer treatment via targeting various cell death pathways. However, the potential of N-SNPs to be usable and biocompatible anticancer drug will depend on their toxicity against normal cells.

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Citreoviridin induces ROS-dependent autophagic cell death in human liver HepG2 cells

Toxicon ◽

10.1016/j.toxicon.2014.12.014 ◽

2015 ◽

Vol 95 ◽

pp. 30-37 ◽

Cited By ~ 16

Author(s):

Ya-Nan Liu ◽

Yue-Xia Wang ◽

Xiao-Fang Liu ◽

Li-Ping Jiang ◽

Guang Yang ◽

...

Keyword(s):

Cell Death ◽

Hepg2 Cells ◽

Human Liver ◽

Autophagic Cell Death

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Effects of VO2 nanoparticles on human liver HepG2 cells: Cytotoxicity, genotoxicity, and glucose and lipid metabolism disorders

NanoImpact ◽

10.1016/j.impact.2021.100351 ◽

2021 ◽

Vol 24 ◽

pp. 100351

Author(s):

Jia-Bei Li ◽

Wen-Song Xi ◽

Shi-Ying Tan ◽

Yuan-Yuan Liu ◽

Hao Wu ◽

...

Keyword(s):

Lipid Metabolism ◽

Hepg2 Cells ◽

Human Liver ◽

Glucose And Lipid Metabolism ◽

Lipid Metabolism Disorders

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Silver Nanoparticles: An Instantaneous Solution for Anticancer Activity against Human Liver (HepG2) and Breast (MCF-7) Cancer Cells

Metals ◽

10.3390/met12010148 ◽

2022 ◽

Vol 12 (1) ◽

pp. 148

Author(s):

Abdulaziz A. Al-Khedhairy ◽

Rizwan Wahab

Keyword(s):

Silver Nanoparticles ◽

Cancer Cells ◽

Human Liver ◽

Quantitative Polymerase Chain Reaction ◽

Cell Types ◽

Whole Body ◽

Low Concentrations ◽

Excellent Control ◽

Mcf 7

Cancer is a cataclysmic disease that affects not only the target organ, but also the whole body. Metal-based nanoparticles (NPs) have recently emerged as a better option for the treatment of this deadly disease. Accordingly, the present work describes a means to control the growth of cancer cells by using colloidal silver nanoparticles (AgNPs) processed via homemade solutions and the characterization of these materials. The AgNPs may become an instantaneous solution for the treatment of these deadly diseases and to minimize or remove these problems. The AgNPs exhibit excellent control of the growth rate of human liver (HepG2) and breast (MCF-7) cancer cells, even at a very low concentrations. The cytotoxic effects of AgNPs on HepG2 and MCF-7 cancer cells were dose dependent (2–200 μg/mL), as evaluated using MTT and NRU assays. The production of reactive oxygen species (ROS) was increased by 136% and 142% in HepG2 and MCF-7 cells treated with AgNPs, respectively. The quantitative polymerase chain reaction (qPCR) data for both cell types (HepG2 and MCF-7) after exposure to AgNPs showed up- and downregulation of the expression of apoptotic (p53, Bax, caspase-3) and anti-apoptotic (BCl2) genes; moreover, their roles were described. This work shows that NPs were successfully prepared and controlled the growth of both types of cancer cells.

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Altered Protein Expressions in Chronic PCB-153–Induced Human Liver (HepG2) Cells

International Journal of Toxicology ◽

10.1080/10915810701352648 ◽

2007 ◽

Vol 26 (3) ◽

pp. 203-212 ◽

Cited By ~ 13

Author(s):

Somiranjan Ghosh ◽

Supriyo De ◽

Sisir K. Dutta

Keyword(s):

Tumor Suppressor ◽

Hepg2 Cells ◽

Chronic Exposure ◽

Human Liver ◽

Environmental Pollutants ◽

Regulator Protein ◽

Blue Growth ◽

Growth Assay ◽

Related Proteins

Polychlorinated biphenyls (PCBs) are a group of persistent and widely distributed environmental pollutants that have various deleterious effects, e.g., neurotoxic, endocrine disruption and reproductive abnormalities, including cancers. Chronic exposure to environmentally hazardous chemicals like PCBs is of great concern to human health. It has been reported earlier that apoptotic proteins change in rats under chronic PCB treatment. It is of importance to determine if chronically exposed human cells develop a different protein expression. In the present study, the authors chronically exposed metabolically competent human liver (HepG2) cells at 50 to 100 μM to examine the role of the well-known environmentally hazardous pollutant non-coplanar 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB-153) to study cell death. After 12 weeks of exposure these cells showed significant changes in apoptotic death in subsequent trypan blue growth assay, fluorescence microscopy, DNA fragmentation, and immunoblotting studies. Interestingly, chronically exposed cells showed marked differences in apoptotic and/or death-related proteins (e.g., Bcl2, Bak, and the pro and active forms of caspase-9, which were up-regulated), in contrast to acutely exposed (i.e., 48-h PCB-153 exposed) cells, which maintained linear growth despite repeated exposures. Similarly, tumor suppressor protein p53, proto-oncogene c- myc, and cell cycle regulator protein p21 were also up-regulated compared to nonchronically exposed HepG2 Cells. The results indicated that PCB-153–induced chronic exposure significantly altered different apoptotic (e.g., Bcl2, Bak, caspase-3) and tumor suppressor (e.g., p21, p53, and c-myc) proteins in the cellular model. These results suggest that chronic exposure to PCB-153 can induce cell survival by altering several apoptotic and tumor suppressor proteins.

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