scholarly journals Effect of Mesenchymal Stem Cells and a Novel Curcumin Derivative on Notch1 Signaling in Hepatoma Cell Line

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Mohamed Talaat Abdel Aziz ◽  
Hussien Mostafa Khaled ◽  
Ali El Hindawi ◽  
Nagwa Kamal Roshdy ◽  
Laila A. Rashed ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Line ◽  
Hepg2 Cells ◽  
Target Genes ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Notch1 Signaling ◽  
Notch1 Signaling Pathway ◽  
Curcumin Derivative

This study was conducted to evaluate the effect of mesenchymal stem cells (MSCs) and a novel curcumin derivative (NCD) on HepG2 cells (hepatoma cell line) and to investigate their effect on Notch1 signaling pathway target genes. HepG2 cells were divided into HepG2 control group, HepG2 cells treated with MSC conditioned medium (MSCs CM), HepG2 cells treated with a NCD, HepG2 cells treated with MSCs CM and NCD, and HepG2 cells treated with MSCs CM (CM of MSCs pretreated with a NCD). Expression of Notch1, Hes1, VEGF, and cyclin D1 was assessed by real-time, reverse transcription-polymerase chain reaction (RT-PCR) in HepG2 cells. In addition, HepG2 proliferation assay was performed in all groups. Notch1 and its target genes (Hes1 and cyclin D1) were downregulated in all treated groups with more suppressive effect in the groups treated with both MSCs and NCD. Also, treated HepG2 cells showed significant decrease in cell proliferation rate. These data suggest that modulation of Notch1 signaling pathway by MSCs and/or NCD can be considered as a therapeutic target in HCC.

scholarly journals Effect of human mesenchymal stem cells on hepatoma cell line

2011 ◽  
Vol 1 (1) ◽  
pp. 12
Author(s):  
Mohamed T. Abdel Aziz ◽  
Hanan H. Fouad ◽  
Nagwa K. Roshdy ◽  
Laila A. Rashed ◽  
Dina Sabry ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Line ◽  
Hepatoma Cell ◽  
Human Mesenchymal Stem Cells ◽  
Hepatoma Cell Line

Comparative cytotoxicity and apoptotic pathways induced by nanosilver in human liver HepG2 and L02 cells

2018 ◽  
Vol 37 (12) ◽  
pp. 1293-1309 ◽  
Author(s):  
Y Xue ◽  
J Wang ◽  
Y Huang ◽  
X Gao ◽  
L Kong ◽  
...  
Keyword(s):  
Cell Line ◽  
Hepg2 Cells ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Hepatoma Cell ◽  
Death Receptor ◽  
Hepatoma Cell Line ◽  
Dependent Manner ◽  
Death Receptor Pathway ◽  
L02 Cells

Silver nanoparticles are used in many commercial products in daily life. Exposure to nanosilver has hepatotoxic effects in animals. This study investigated the cytotoxicity associated with polyvinylpyrrolidone-coated nanosilver (23.44 ± 4.92 nm in diameter) exposure in the human hepatoma cell line (HepG2) and normal hepatic cell line (L02), and the molecular mechanisms induced by nanosilver in HepG2 cells. Nanosilver, in doses of 20–160 μg mL−1 for 24 and 48 h, reduced cell viability in a dose- and time-dependent manner and induced cell membrane leakage and mitochondria injury in both cell lines; these effects were more pronounced in HepG2 cells than in L02 cells. Intracellular oxidative stress was documented by reactive oxygen species (ROS) being generated in HepG2 cells but not in L02 cells, an effect possibly due to differential uptake of nanosilver by cancer cells and normal cells. In HepG2 cells, apoptosis was documented by finding that ROS triggered a decrease in mitochondrial membrane potential, an increase in cytochrome c release, activation of caspase 3 and caspase 9, and a decrease in the ratio of Bcl-2/Bax. Furthermore, nanosilver activated the Fas death receptor pathway by downregulation of nuclear factor-κB and activation of caspase 8 and caspase 3. These results suggest that apoptosis induced by nanosilver in HepG2 cells is mediated via a mitochondria-dependent pathway and the Fas death receptor pathway. These findings provide toxicological and mechanistic information that can help in assessing the effects of nanosilver in biological systems, including the potential for anticancer activities.

scholarly journals Selective Attenuation of Metabolic Branch of Insulin Receptor Down-signaling by High Glucose in a Hepatoma Cell Line, HepG2 Cells

2000 ◽  
Vol 275 (27) ◽  
pp. 20880-20886 ◽  
Author(s):  
Koji Nakajima ◽  
Keishi Yamauchi ◽  
Satoshi Shigematsu ◽  
Sachiko Ikeo ◽  
Mitsuhisa Komatsu ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
Cell Line ◽  
High Glucose ◽  
Hepg2 Cells ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Hepatoma Cell Line Hepg2

Cytotoxicity, genotoxicity and oxidative reactions in cell-culture models: modulatory effects of phytochemicals

2000 ◽  
Vol 28 (2) ◽  
pp. 22-26 ◽  
Author(s):  
N. M. O'Brien ◽  
J. A. Woods ◽  
S. A. Aherne ◽  
Y. C. O'Callaghan
Keyword(s):  
Dna Damage ◽  
Cell Line ◽  
Hepg2 Cells ◽  
Biological Effects ◽  
Hepatoma Cell ◽  
Radical Scavenging ◽  
Hepatoma Cell Line ◽  
Beneficial Effects ◽  
Cellular Models ◽  
Oxidative Reactions

Much research effort has focused on the identification of phytochemicals in fruit and vegetables which exert beneficial effects. Our research examines modulatory effects of phytochemicals on cytotoxicity, genotoxicity and oxidative reactions in cell systems. Two examples of our studies are discussed. First, the potential beneficial effects of flavonoids are demonstrated. Flavonoids are reported to exhibit a wide variety of biological effects, including antioxidant and free-radical-scavenging activities. The aim of the study was to determine if flavonoids could protect against H2O2-induced DNA damage, as measured by the comet assay, in Caco-2 and HepG2 cells. Both cell lines were supplemented with increasing concentrations of myricetin, quercetin and rutin for 24 h followed by exposure to H2O2 (50 μM) for 30 min. Exposure to H2O2 for 30 min at 37 °C resulted in significant DNA damage and pre-incubation with the flavonoids before H2O2 exposure significantly (P <0.05) protected Caco-2 and HepG2 cells against H2O2-induced DNA damage. Secondly, we illustrate the use of cellular models to study oxysterol-induced toxicity. Oxy-sterols are generated during the cooking and processing of foods and may be produced endogenously by the oxidation of membrane lipids. Recent findings suggest that oxysterols may modulate cytotoxicity by exerting effects on the induction of apoptosis. 7β-Hydroxycholesterol (7β-OHC) and 25-hydroxycholesterol, both of which are commonly found in foods, were investigated for their abilities to induce apoptosis in a human monocytic blood cell line, U937, and in the human hepatoma cell line, HepG2 cells. U937 and HepG2 cells were incubated for up to 48 h with 30 μM oxysterol. 7β-OHC induced apoptosis in U937 cells as measured by non-random DNA fragmentation, condensed and fragmented nuclei, and the generation of hypodiploid cells. In contrast, oxysterols may induce cell death by a different mechanism in the hepatoma cells, possibly by necrosis.

scholarly journals Suitability of hepatocyte cell lines HepG2, AML12 and THLE-2 for investigation of insulin signalling and hepatokine gene expression

Open Biology ◽  
2018 ◽  
Vol 8 (10) ◽  
pp. 180147 ◽  
Author(s):  
Stephanie Sefried ◽  
Hans-Ulrich Häring ◽  
Cora Weigert ◽  
Sabine S. Eckstein
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Hepg2 Cells ◽  
Insulin Signalling ◽  
Hepatoma Cell ◽  
Human Cell Line ◽  
Hepatoma Cell Line ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Immortal hepatocyte cell lines are widely used to elucidate insulin-dependent signalling pathways and regulation of hepatic metabolism, although the often tumorigenic origin might not represent the metabolic state of healthy hepatocytes. We aimed to investigate if murine cell line AML12 and human cell line THLE-2, which are derived from healthy liver cells, are comparable to hepatoma cell line HepG2 for studying acute insulin signalling and expression of gluconeogenic enzymes and hepatokines. Insulin responsiveness of AML12 and THLE-2 cells was impaired when cells were cultured in the recommended growth medium, but comparable with HepG2 cells by using insulin-deficient medium. THLE-2 cells showed low abundance of insulin receptor, while protein levels in HepG2 and AML12 were comparable. AML12 and THLE-2 cells showed only low or non-detectable transcript levels of G6PC and PCK1 . Expression of ANGPTL4 was regulated similarly in HepG2 and AML12 cells upon peroxisome proliferator-activated receptor δ activation but only HepG2 cells resemble the in vivo regulation of hepatic ANGPTL4 by cAMP. Composition of the culture medium and protein expression levels of key signalling proteins should be considered when AML12 and THLE-2 are used to study insulin signalling. With regard to gluconeogenesis and hepatokine expression, HepG2 cells appear to be closer to the in vivo situation despite the tumorigenic origin.

Solena amplexicaulis Induces Cell Cycle Arrest, Apoptosis and Inhibits Angiogenesis in Hepatocarcinoma Cells and HUVECs

2014 ◽  
Vol 42 (06) ◽  
pp. 1521-1537 ◽  
Author(s):  
Jie Ren ◽  
Yuan Yuan Xu ◽  
He Fei Jiang ◽  
Meng Yang ◽  
Qian Hui Huang ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Cell Apoptosis ◽  
Hepg2 Cells ◽  
Hepatoma Cell ◽  
Endothelial Cell Migration ◽  
Hepatoma Cell Line ◽  
Dependent Manner ◽  
Solena Amplexicaulis ◽  
Protein Expressions

Solena amplexicaulis (Lam.) Gandhi (SA) has been used as a traditional medicine for the treatment of dysentery, multiple abscess, gastralgia, urethritis, and eczema in the minority area of China. This study was aimed to examine the cell proliferation inhibitory activity of the SA extract (SACE) and its mechanism of action in human hepatoma cell line (HepG2) and evaluate its anti-angiogenesis activity in human umbilical vein endothelial cell line (HUVEC). SACE could inhibit the growth of HepG2 cells in a dose- and time-dependent manner. FCM analysis showed that SACE could induce G2/M phase arrest, cell apoptosis, the mitochondrial membrane potential loss (ΔΨm) and increase the production of intracellular ROS of HepG2 cells. After treatment with SACE, topical morphological changes of apoptotic body formation, obvious increase of apoptosis-related protein expressions, such as Bax, cytochrome c, caspase-3, PARP-1, and decrease of Bcl-2, procaspase-9 protein expressions were observed at the same time. Moreover, SACE caused the significant inhibition of endothelial cell migration and tube formation in HUVEC cells. The results suggested that SACE could act as an angiogenesis inhibitor and induce cell apoptosis via a caspase-dependent mitochondrial pathway. Therefore, SACE could be a potent candidate for the prevention and treatment of liver cancer.

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