scholarly journals Veronicastrum axillareAlleviates Ethanol-Induced Injury on Gastric Epithelial Cells via Downregulation of the NF-kB Signaling Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Wei-chun Zhao ◽  
Yan-shan Xu ◽  
Gang Chen ◽  
Yan Guo ◽  
Dan-yi Wang ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Epithelial Cells ◽  
Protective Effect ◽  
Cell Viability ◽  
Cell Damage ◽  
Damage Model ◽  
Signal Pathway ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gastric Epithelial Cells ◽  
Chronic Nephritis

We used human gastric epithelial cells (GES-1) line in an ethanol-induced cell damage model to study the protective effect ofVeronicastrum axillareand its modulation to NF-κB signal pathway. The goal was to probe the molecular mechanism ofV. axillaredecoction in the prevention of gastric ulcer and therefore provide guidance in the clinical application ofV. axillareon treating injuries from chronic nephritis, pleural effusion, gastric ulcer, and other ailments. The effects ofV. axillare-loaded serums on cell viability were detected by MTT assays. Enzyme-linked immunosorbent assay (ELISA) and Real-Time PCR methods were used to analyze the protein and mRNA expression of TNF-α, NF-κB, IκBα, and IKKβ. The results showed thatV. axillare-loaded serum partially reversed the damaging effects of ethanol and NF-κB activator (phorbol-12-myristate-13-acetate: PMA) and increased cell viability. The protein and mRNA expressions of TNF-α, NF-κB, IκBα, and IKKβwere significantly upregulated by ethanol and PMA while they were downregulated byV. axillare-loaded serum. In summary,V. axillare-loaded serum has significantly protective effect on GES-1 against ethanol-induced injury. The protective effect was likely linked to downregulation of TNF-αbased NF-κB signal pathway.

scholarly journals Rabeprazole inhibits inflammatory reaction by inhibition of cell pyroptosis in gastric epithelial cells

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Jing Xie ◽  
Long Fan ◽  
Liya Xiong ◽  
Peiyu Chen ◽  
Hongli Wang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Clinical Sample ◽  
Critical Role ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammasome Activation ◽  
Peptic Ulcers ◽  
Gastric Epithelial Cells ◽  
Caspase 1 ◽  
H Pylori

Abstract Background Helicobacter pylori (H. pylori) is a common pathogen in development of peptic ulcers with pyroptosis. Rabeprazole, a critical component of standard triple therapy, has been widely used as the first-line regimen for H. pylori infectious treatment. The aim of this study to explore the function of Rabeprazole on cell pyroptosis in vitro. Methods The clinical sample from patients diagnosed with or without H. pylori-infection were collected to analyze by Immunohistochemistry (IHC). Real-time quantitative PCR (qPCR), western blot (WB) and enzyme linked immunosorbent assay (Elisa) were performed to analyze the effect of Rabeprazole on cell pyroptosis, including LDH, IL-1β and IL-18. Results In this study, we showed that Rabeprazole regulated a phenomenon of cell pyroptosis as confirmed by lactate dehydrogenase (LDH) assay. Further results showed that Rabeprazole inhibited cell pyroptosis in gastric epithelial cells by alleviating GSDMD-executed pyroptosis, leading to decrease IL-1β and IL-18 mature and secretion, which is attributed to NLRP3 inflammasome activation inhibition. Further analysis showed that ASC, NLRP3 and Caspase-1, was significantly repressed in response to Rabeprazole stimulation, resulting in decreasing cleaved-caspase-1 expression. Most important, NLRP3 and GSDMD is significantly increased in gastric tissue of patients with H. pylori infection. Conclusion These findings revealed a critical role of Rabeprazole in cell pyroptosis in patients with H. pylori infection, suggesting that targeting cell pyroptosis is an alternative strategy in improving H. pylori treatment.

The protective effect of rebamipide on paracellular permeability of rat gastric epithelial cells

2003 ◽  
Vol 18 ◽  
pp. 133-138 ◽  
Author(s):  
T. Joh ◽  
Y. Takezono ◽  
T. Oshima ◽  
M. Sasaki ◽  
K. Seno ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protective Effect ◽  
Paracellular Permeability ◽  
Gastric Epithelial Cells

Antisense oligodeoxynucleotides to inducible NO synthase rescue epithelial cells from oxidative stress injury

1996 ◽  
Vol 270 (6) ◽  
pp. F971-F977 ◽  
Author(s):  
T. Peresleni ◽  
E. Noiri ◽  
W. F. Bahou ◽  
M. S. Goligorsky
Keyword(s):  
Epithelial Cells ◽  
Cell Viability ◽  
Cell Damage ◽  
Oxidant Stress ◽  
Selective Inhibition ◽  
Stress Injury ◽  
Cytoplasmic Staining ◽  
Nitrite Production ◽  
Stressed Cells ◽  
Antisense Odns

Until recently, the lack of specific inhibitors of various forms of nitric oxide synthase (NOS) hampered a stringent evaluation of the role played by inducible NOS (iNOS) in cell damage. Phosphorothioate derivatives of iNOS antisense and control sense or scrambled oligodeoxynucleotides (S-ODNs) were synthesized, and their effect on epithelial cell viability was examined under oxidant stress. Exposure of BSC-1 kidney tubular epithelial cells to H2O2 resulted in elevation of NO release, accompanied by a significant decrease in the population of viable cells (from 97.4 +/- 1.7% to 72.4 +/- 2.4% population). Nitrite production by BSC-1 cells exposed to H2O2 increased almost 10-fold compared with control. Pretreatment of the cells with 10 microM antisense ODNs significantly blunted this response, whereas sense or scrambled ODNs did not modify it. Pretreatment of BSC-1 cells with 10 microM antisense ODNs virtually prevented lethal cell damage in response to H2O2, whereas sense ODNs were ineffective. Lipopolysaccharide induction of iNOS, also preventable by the antisense construct, resulted in a lesser compromise to cell viability. Immunocytochemistry of iNOS in cells pretreated with antisense ODNs showed minimal cytoplasmic staining, as opposed to the untreated or sense ODN-treated positively stained cells. Staining with antibodies to nitrotyrosine was conspicuous in stressed cells but undetectable in antisense ODN-treated cells. In conclusion, oxidant stress is accompanied by the induction of iNOS, increased production of NO, and impaired cell viability; selective inhibition of iNOS using the designed antisense ODNs dramatically improved BSC-1 cell viability after oxidant stress.

scholarly journals NSAID-induced injury of gastric epithelial cells is reversible: roles of mitochondria, AMP kinase, NGF, and PGE2

2019 ◽  
Vol 317 (6) ◽  
pp. G862-G871
Author(s):  
Amrita Ahluwalia ◽  
Neil Hoa ◽  
Michael K. Jones ◽  
Andrzej S. Tarnawski
Keyword(s):  
Membrane Potential ◽  
Nerve Growth Factor ◽  
Epithelial Cells ◽  
Cell Viability ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Cell Injury ◽  
Prostaglandin E ◽  
Gastric Epithelial Cells ◽  
Amp Kinase

Nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac (DFN) and indomethacin (INDO) are extensively used worldwide. Their main side effects are injury of the gastrointestinal tract, including erosions, ulcers, and bleeding. Since gastric epithelial cells (GEPCs) are crucial for mucosal defense and are the major target of injury, we examined the extent to which DFN- and INDO-induced GEPC injury can be reversed by nerve growth factor (NGF), 16,16 dimethyl prostaglandin E2 (dmPGE2), and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), the pharmacological activator of the metabolic sensor AMP kinase (AMPK). Cultured normal rat gastric mucosal epithelial (RGM1) cells were treated with PBS (control), NGF, dmPGE2, AICAR, and/or NSAID (DFN or INDO) for 1–4 h. We examined cell injury by confocal microscopy, cell death/survival using calcein AM, mitochondrial membrane potential using MitoTracker, and phosphorylation of AMPK by Western blotting. DFN and INDO treatment of RGM1 cells for 2 h decreased mitochondrial membrane potential and cell viability. NGF posttreatment (initiated 1 or 2 h after DFN or INDO) reversed the dissipation of mitochondrial membrane potential and cell injury caused by DFN and INDO and increased cell viability versus cells treated for 4 h with NSAID alone. Pretreatment with dmPGE2 and AICAR significantly protected these cells from DFN- and INDO-induced injury, whereas dmPGE2 and AICAR posttreatment (initiated 1 h after NSAID treatment) reversed cell injury and significantly increased cell viability and rescued the cells from NSAID-induced mitochondrial membrane potential reduction. DFN and INDO induce extensive mitochondrial injury and GEPC death, which can be significantly reversed by NGF, dmPGE2, and AICAR. NEW & NOTEWORTHY This study demonstrated that mitochondria are key targets of diclofenac- and indomethacin-induced injury of gastric epithelial cells and that diclofenac and indomethacin injury can be prevented and, importantly, also reversed by treatment with nerve growth factor, 16,16 dimethyl prostaglandin E2, and 5-aminoimidazole-4-carboxamide ribonucleotide.

scholarly journals Antioxidant Effects and Cytoprotective Potentials of Herbal Tea against H2O2-Induced Oxidative Damage by Activating Heme Oxygenase1 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Ke-Xin Zhang ◽  
Jian-Bin Tan ◽  
Cheng-Liang Xie ◽  
Rong-Bo Zheng ◽  
Xiao-Dan Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Protective Effect ◽  
Functional Foods ◽  
Cell Damage ◽  
Damage Model ◽  
Enrichment Analysis ◽  
Protective Effects ◽  
Herbal Tea ◽  
Antioxidant Effects

Herbal tea with antioxidant ingredients has gained increasing attention in the field of functional foods due to their amelioration potential in aging-related diseases. Wanglaoji herbal tea (WHT) is a kind of traditional beverage made from herbal materials. This study was performed to investigate its antioxidant activity and identify its protective effect on a H2O2-induced cell damage model. In this study, we identified six kinds of phenolic acids with antioxidant activity in WHT, among which rosmarinic acid had the highest content and the highest contribution ratio to the antioxidant activity of WHT. Moreover, compared with the H2O2-induced damage group, the WHT treatment group can significantly increase the viability of cells and decrease the ratio of senescence-associated β-galactosidase-positive cells, intracellular malondialdehyde levels, and the percentage of G1 phase. Furthermore, enrichment analysis of differentially expressed genes revealed that heme oxygenase1 (HMOX1) was a key gene for protective effect of WHT on oxidative stress-induced cell damage. Thus, WHT exerted protective effects not only by scavenging reactive oxygen species but also by inducing the expression of cytoprotective genes by activating the HMOX1 pathway, which showed that WHT had a potential of promoting health by reducing oxidative stress-induced cell damage.

Protective effect of carbachol postconditioning on hypoxia/reoxygenation-induced injury in human gastric epithelial cells

Life Sciences ◽  
2016 ◽  
Vol 144 ◽  
pp. 234-242 ◽  
Author(s):  
Hongxia Han ◽  
Jun Yang ◽  
Sujuan Fei ◽  
Zhangbo Liu ◽  
Shengping Zhu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protective Effect ◽  
Gastric Epithelial Cells ◽  
Hypoxia Reoxygenation

scholarly journals Cytokine Expression and Production by Purified Helicobacter pylori Urease in Human Gastric Epithelial Cells

2000 ◽  
Vol 68 (2) ◽  
pp. 664-671 ◽  
Author(s):  
Toshihito Tanahashi ◽  
Masakazu Kita ◽  
Tadashi Kodama ◽  
Yoshio Yamaoka ◽  
Naoki Sawai ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Proinflammatory Cytokines ◽  
Gastric Cancer Cell Line ◽  
Mucosal Inflammation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gastric Epithelial Cells ◽  
Cytokine Induction ◽  
H Pylori ◽  
Stimulation Of

ABSTRACT Cytokines have been proposed to play an important role inHelicobacter pylori-associated gastroduodenal diseases, but the exact mechanism of the cytokine induction remains unclear. H. pylori urease, a major component of the soluble proteins extracted from bacterial cells, is considered to be one of the virulence factors for the inflammation in the gastric mucosa that is produced in H. pylori infection. However, the response of human gastric epithelial cells to the stimulation of urease has not been investigated. In the present study, we used human gastric epithelial cells in a primary culture system and examined whetherH. pylori urease stimulates the gastric epithelial cells to induce proinflammatory cytokines by reverse transcription-PCR and enzyme-linked immunosorbent assay. First, by using peripheral blood mononuclear cells (PBMC) and a gastric cancer cell line (MKN-45 cells), we confirmed the ability of purified H. pylori urease to induce the production of proinflammatory cytokines. Furthermore, we demonstrated that the human gastric epithelial cells produced interleukin-6 (IL-6) and tumor necrosis factor alpha, but not IL-8, following stimulation with purified urease. The patterns of cytokine induction differed among human PBMC, MKN-45 cells, and human gastric epithelial cells. These results suggest that the human gastric epithelial cells contribute to the induction of proinflammatory cytokines by the stimulation of H. pylori urease, indicating that the epithelial cells were involved in the mucosal inflammation that accompanied H. pylori infection.

scholarly journals Protective Activity of Aspirin Eugenol Ester on Paraquat-Induced Cell Damage in SH-SY5Y Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Zhen-Dong Zhang ◽  
Ya-Jun Yang ◽  
Zhe Qin ◽  
Xi-Wang Liu ◽  
Shi-Hong Li ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cell Viability ◽  
Caspase 3 ◽  
Cell Damage ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Human Neuroblastoma ◽  
Aspirin Eugenol Ester

Aspirin eugenol ester (AEE) is a new pharmaceutical compound esterified by aspirin and eugenol, which has anti-inflammatory, antioxidant, and other pharmacological activities. The aim of this study was to investigate the protective effect of AEE on paraquat- (PQ-) induced cell damage of SH-SY5Y human neuroblastoma cells and its potential molecular mechanism. There was no significant change in cell viability when AEE was used alone. PQ treatment reduced cell viability in a concentration-dependent manner. However, AEE reduced the PQ-induced loss of cell viability. Flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and 4 ′ 6-diamidino-2-phenylindole (DAPI) staining were used to evaluate cell apoptosis. Compared with the PQ group, AEE pretreatment could significantly inhibit PQ-induced cell damage. AEE pretreatment could reduce the cell damage of SH-SY5Y cells induced by PQ via reducing superoxide anion, intracellular reactive oxygen species (ROS), and mitochondrial ROS (mtROS) and increasing the levels of mitochondrial membrane potential ( Δ Ψ m ). At the same time, AEE could increase the activity of glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD) and decrease the activity of malondialdehyde (MDA). The results showed that compared with the control group, the expression of p-PI3K, p-Akt, and Bcl-2 was significantly decreased, while the expression of caspase-3 and Bax was significantly increased in the PQ group. In the AEE group, AEE pretreatment could upregulate the expression of p-PI3K, p-Akt, and Bcl-2 and downregulate the expression of caspase-3 and Bax in SH-SY5Y cells. PI3K inhibitor LY294002 and the silencing of PI3K by shRNA could weaken the protective effect of AEE on PQ-induced SH-SY5Y cells. Therefore, AEE has a protective effect on PQ-induced SH-SY5Y cells by regulating the PI3K/Akt signal pathway to inhibit oxidative stress.

Sign in / Sign up

Export Citation Format

Share Document