scholarly journals Anti-inflammatory Effects of Alcohol Are Associated with JNK-STAT3 Downregulation in an In Vitro Inflammation Model in HepG2 Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Katharina Mörs ◽  
Ramona Sturm ◽  
Jason-Alexander Hörauf ◽  
Shinwan Kany ◽  
Paola Cavalli ◽  
...  
Keyword(s):  
Hepg2 Cells ◽  
Acute Inflammation ◽  
In Vitro Model ◽  
Prolonged Exposure ◽  
Acute Exposure ◽  
High Dose ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Vitro Model

Background. In several preclinical and in vitro models of acute inflammation, alcohol (ethanol, EtOH) has been described as an immunomodulatory agent. Similarly, in different pathologies, clinical observations have confirmed either pro- or anti-inflammatory effects of EtOH. The liver plays an important role in immunity and alcohol metabolism; therefore, we analysed dose- and time-dependent effects of EtOH on the inflammatory response of human liver cells in an in vitro model of acute inflammation. Methods. HepG2 cells were stimulated with IL-1β and subsequently exposed to EtOH in a low or high dose (85 mM, LoD or 170 mM, HiD) for 1 h (acute exposure) or 72 h (prolonged exposure). IL-6 and TNF-α release was determined by ELISA. Cell viability, adhesion of isolated neutrophils to HepG2 monolayers, their ICAM-1 expression, and the activation of stress-induced protein kinase/c-Jun N-terminal kinase (SAPK/JNK) or signal transducer and activator of transcription 3 (STAT3) were analysed. Results. In this experimental design, EtOH did not markedly change the cell viability. Acute and prolonged exposure to EtOH significantly reduced dose-independent IL-1β-induced IL-6 and TNF-α release, as well as adhesion capacity to pretreated HepG2 cells. Acute exposure to EtOH significantly decreased the percentage of ICAM-1-expressing cells. IL-1β stimulation notably increased the activation of SAPK/JNK. However, low-dose EtOH exposure reduced this activation considerably, in contradiction to high-dose EtOH exposure. Acute exposure to LoD EtOH significantly diminished the IL-1β-induced STAT3 activation, whereas an acute exposure of cells to either HiD EtOH or in a prolonged setting showed no effects on STAT3 activation. Conclusion. EtOH exerts anti-inflammatory potential in this in vitro model of hepatic inflammation. These effects are associated with the reduced activation of JNK/STAT3 by EtOH, particularly in the condition of acute exposure to low-dose EtOH.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

AAnti-Inflammatory Effects of Plasma Circulating Exosomes Obtained from Normal-Weight and Obese Subjects on Hepatocytes

2020 ◽  
Vol 20 ◽  
Author(s):  
Reza Afrisham ◽  
Sahar Sadegh-Nejadi ◽  
Reza Meshkani ◽  
Solaleh Emamgholipour ◽  
Molood Bagherieh ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Liver Cells ◽  
Normal Weight ◽  
Protein Levels ◽  
Human Liver Cells ◽  
Tnf Α ◽  
Anti Inflammatory

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.

Development of in vitro model of insulin receptor cleavage induced by high glucose in HepG2 cells

2014 ◽  
Vol 445 (1) ◽  
pp. 236-243 ◽  
Author(s):  
Tomoyuki Yuasa ◽  
Kikuko Amo ◽  
Shuhei Ishikura ◽  
Hisao Nagaya ◽  
Keiji Uchiyama ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
High Glucose ◽  
Hepg2 Cells ◽  
In Vitro Model ◽  
Vitro Model

Anti-inflammatory effects of dietary phenolic compounds in an in vitro model of inflamed human intestinal epithelium

2010 ◽  
Vol 188 (3) ◽  
pp. 659-667 ◽  
Author(s):  
Thérèse Sergent ◽  
Neil Piront ◽  
Julie Meurice ◽  
Olivier Toussaint ◽  
Yves-Jacques Schneider
Keyword(s):  
Phenolic Compounds ◽  
Intestinal Epithelium ◽  
In Vitro Model ◽  
Anti Inflammatory ◽  
Vitro Model ◽  
Human Intestinal Epithelium

Beneficial effects of nontoxic ozone on H2O2-induced stress and inflammation

2016 ◽  
Vol 94 (6) ◽  
pp. 577-583 ◽  
Author(s):  
Altug Kucukgul ◽  
Suat Erdogan ◽  
Ramazan Gonenci ◽  
Gonca Ozan
Keyword(s):  
Cell Loss ◽  
Alveolar Cells ◽  
Sod Activity ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Ozone Pretreatment ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Vitro Model

In this study, the anti-oxidant and anti-inflammatory efficacy of ozone oxidative preconditioning (OOP) were investigated on hydrogen peroxide (H2O2)-induced human lung alveolar cells. In MTT and trypan blue viability tests, while 100 μmol/L H2O2caused a 17.3% and 21.9% decrease in the number of living cells, respectively, ozone at 20 μmol/L regenerated cell proliferation and prevented 9.6% and 11.0% of cell loss, respectively. In addition, H2O2decreased the transcription levels of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) 5.43-, 2.89-, and 5.33-fold, respectively, while it increased Bax, NF-κβ, TNF-α, and iNOS expression 1.57-, 1.32-, 1.40-, and 1.41-fold, respectively. Ozone pretreatment, however, increased CAT, GPx, and SOD transcription levels 7.08-, 5.17-, and 6.49-fold and decreased Bax, NF-κβ, TNF-α, and iNOS transcriptions by 1.25-, 0.76-, 3.63-, and 7.91-fold, respectively. Moreover, intracellular glutathione (GSH) level and SOD activity were decreased by 46.2% and 45.0% in the H2O2treatment group, and OOP recovered 58.5% and 20.1% of the decreases caused by H2O2. H2O2also increased nitrite levels 7.84-fold, and OOP reduced this increase by half. Consequently, OOP demonstrated potent anti-oxidant and anti-inflammatory effects on in vitro model of oxidative stress-induced lung injury.

TNF-α Induces MMP2 Gelatinase Activity and MT1-MMP Expression in an In Vitro Model of Nucleus Pulposus Tissue Degeneration

Spine ◽  
2008 ◽  
Vol 33 (4) ◽  
pp. 356-365 ◽  
Author(s):  
Cheryle A. Séguin ◽  
Robert M. Pilliar ◽  
Joseph A. Madri ◽  
Rita A. Kandel
Keyword(s):  
Nucleus Pulposus ◽  
In Vitro Model ◽  
Gelatinase Activity ◽  
Nucleus Pulposus Tissue ◽  
Tissue Degeneration ◽  
Tnf Α ◽  
Vitro Model

HepG2 cells as an in vitro model for evaluation of cytochrome P450 induction by xenobiotics

2014 ◽  
Vol 38 (5) ◽  
pp. 691-704 ◽  
Author(s):  
Jong Min Choi ◽  
Soo Jin Oh ◽  
Sang Yoon Lee ◽  
Ji Hye Im ◽  
Jung Min Oh ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Hepg2 Cells ◽  
In Vitro Model ◽  
Cytochrome P450 Induction ◽  
Vitro Model
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