scholarly journals Alkaline Reduced Water Attenuates Oxidative Stress-Induced Mitochondrial Dysfunction and Innate Immune Response Triggered by Intestinal Epithelial Dysfunction

Processes ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1828
Author(s):  
Jayson M. Antonio ◽  
Ailyn Fadriquela ◽  
Yun Ju Jeong ◽  
Cheol-Su Kim ◽  
Soo-Ki Kim
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Mitochondrial Dysfunction ◽  
Intestinal Epithelial Cells ◽  
Intestinal Barrier ◽  
Mapk Signaling ◽  
Raw 264.7 Cells ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Reduced Water

Redox imbalance in intestinal epithelial cells is critical in the early phases of intestinal injury. Dysfunction of the intestinal barrier can result in immunological imbalance and inflammation, thus leading to intestinal syndromes and associated illnesses. Several antioxidants have been discovered to be beneficial in resolving intestinal barrier dysfunction. Of these antioxidants, the effects of alkaline reduced water (ARW) in oxidative stress of intestinal epithelial cells and its immunokine modulation in vitro is unknown. In this study, we utilized ARW-enriched media to investigate its cytoprotective effect against H2O2-induced oxidative stress in DLD1 cells. We found that ARW rescued DLD1 from oxidative stress by diluting the influence of H2O2 on oxidative stress-activated MAPK signaling and mitochondrial dysfunction. Further, intestinal oxidative stress significantly affects immunokine profiles of Raw 264.7 cells (IL-6, IL-10, MCP, TNF-a, RANTES), which can be reversed by ARW. Collectively, ARW shields intestinal epithelial cells from oxidative stress, reducing the immunological mayhem caused by barrier failure.

scholarly journals Schisandrin A protects intestinal cells from mycophenolic acid-induced cytotoxicity and oxidative damage

2021 ◽  
Author(s):  
Yiyun Deng ◽  
Zhe Zhang ◽  
Yuanyuan Hong ◽  
Lijuan Feng ◽  
Yong Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Oxidative Damage ◽  
Mycophenolic Acid ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
Mapk Signaling ◽  
Intestinal Epithelial

Abstract Objectives: The gastrointestinal side effects of mycophenolic acid affect its efficacy in kidney transplant patients, which may be due to its toxicity to the intestinal epithelial mechanical barrier, including intestinal epithelial cell apoptosis and destruction of tight junctions. The toxicity mechanism of mycophenolic acid is related to oxidative stress-mediated the activation of mitogen-activated protein kinases (MAP K). Schisandrin A (Sch A), one of the main active components of the Schisandra chinensis, can protects intestinal epithelial cells from deoxynivalenol-induced cytotoxicity and oxidative damage by antioxidant effects. The aim of this study was to investigate the protective effect and potential mechanism of Sch A on mycophenolic acid-induced damage in intestinal epithelial cell. Methods: Caco-2 cells monolayers were treated with mycophenolic acid (10µM) and/or Sch A (10, 20 and 40µM) at 37°C for 24h, and cell viability was measured by MTT; Western blot and immunofluorescence were used to detect the expression of relevant proteins. Intracellular ROS and apoptosis were measured by flow cytometry, and malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured by kits. Results: The results showed that Sch A significantly reversed the mycophenolic acid-induced cell viability reduction, restored the expression of tight junction protein ZO-1, occludin and reduced cell apoptosis. In addition, Sch A inhibited mycophenolic acid-mediated MAPK activation and reactive oxygen species (ROS) increase. Conclusions: Sch A protected intestinal epithelial cells from mycophenolic acid intestinal toxicity, at least in part, by reducing oxidative stress and inhibiting MAPK signaling pathway. Conclusions: Sch A protected intestinal epithelial cells from mycophenolic acid intestinal toxicity, at least in part, by reducing oxidative stress and inhibiting MAPK signaling pathway.

scholarly journals Mesenchymal stem cell-derived microvesicles improve intestinal barrier function by restoring mitochondrial dynamic balance in sepsis rats

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Danyang Zheng ◽  
Henan Zhou ◽  
Hongchen Wang ◽  
Yu Zhu ◽  
Yue Wu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Dynamic Balance ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Mitochondrial Dynamic ◽  
Intestinal Barrier Dysfunction

Abstract Background Sepsis is a major cause of death in ICU, and intestinal barrier dysfunction is its important complication, while the treatment is limited. Recently, mesenchymal stem cell-derived microvesicles (MMVs) attract much attention as a strategy of cell-free treatment; whether MMVs are therapeutic in sepsis induced-intestinal barrier dysfunction is obscure. Methods In this study, cecal ligation and puncture-induced sepsis rats and lipopolysaccharide-stimulated intestinal epithelial cells to investigate the effect of MMVs on intestinal barrier dysfunction. MMVs were harvested from mesenchymal stem cells and were injected into sepsis rats, and the intestinal barrier function was measured. Afterward, MMVs were incubated with intestinal epithelial cells, and the effect of MMVs on mitochondrial dynamic balance was measured. Then the expression of mfn1, mfn2, OPA1, and PGC-1α in MMVs were measured by western blot. By upregulation and downregulation of mfn2 and PGC-1α, the role of MMVs in mitochondrial dynamic balance was investigated. Finally, the role of MMV-carried mitochondria in mitochondrial dynamic balance was investigated. Results MMVs restored the intestinal barrier function by improving mitochondrial dynamic balance and metabolism of mitochondria. Further study revealed that MMVs delivered mfn2 and PGC-1α to intestinal epithelial cells, and promoted mitochondrial fusion and biogenesis, thereby improving mitochondrial dynamic balance. Furthermore, MMVs delivered functional mitochondria to intestinal epithelial cells and enhanced energy metabolism directly. Conclusion MMVs can deliver mfn2, PGC-1α, and functional mitochondria to intestinal epithelial cells, synergistically improve mitochondrial dynamic balance of target cells after sepsis, and restore the mitochondrial function and intestinal barrier function. The study illustrated that MMVs might be a promising strategy for the treatment of sepsis.

scholarly journals Beneficial Effect of a Fermented Wheat Germ Extract in Intestinal Epithelial Cells in case of Lipopolysaccharide-Evoked Inflammation

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Z. Karancsi ◽  
A. V. Móritz ◽  
N. Lewin ◽  
A. M. Veres ◽  
Á. Jerzsele ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Wheat Germ ◽  
Intestinal Epithelial Cells ◽  
Intestinal Barrier ◽  
Intestinal Epithelial ◽  
Wheat Germ Extract ◽  
Amplex Red ◽  
Intracellular Ros ◽  
Fermented Wheat Germ Extract

In this study, the protective effect of a fermented wheat germ extract (FWGE) against LPS-induced inflammation and oxidative stress in IPEC-J2 porcine intestinal epithelial cells was studied. Enterocytes were treated with LPS derived from Salmonella enterica ser. Typhimurium and Escherichia coli O55:B5, O111:B4, and O127:B8 strains. Intracellular ROS level and extracellular H2O2 level were followed up by two fluorescent assays (DCFH-DA and Amplex Red). The effect of FWGE on the intestinal barrier integrity was determined by transepithelial electric resistance measurements and using a FD4 fluorescent tracer dye. IL-6 concentration of supernatants was also measured by the ELISA method. Our data revealed that FWGE had a significant lowering effect on the inflammatory response especially related to oxidative stress. Treatment with FWGE (1-2%) significantly decreased the level of intracellular ROS compared to LPS-treated cells. Furthermore, LPS-triggered partial disruption of epithelial integrity was reduced after FWGE application.

scholarly journals Spirulina Crude Protein Promotes the Migration and Proliferation in IEC-6 Cells by Activating EGFR/MAPK Signaling Pathway

Marine Drugs ◽  
2019 ◽  
Vol 17 (4) ◽  
pp. 205
Author(s):  
Su-Jin Jeong ◽  
Jeong-Wook Choi ◽  
Min-Kyeong Lee ◽  
Youn-Hee Choi ◽  
Taek-Jeong Nam
Keyword(s):  
Cell Cycle ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Crude Protein ◽  
Cell Cycle Progression ◽  
Intestinal Epithelial Cells ◽  
Mapk Signaling ◽  
S Phase ◽  
Intestinal Epithelial ◽  
Cycle Progression

Spirulina is a type of filamentous blue-green microalgae known to be rich in nutrients and to have pharmacological effects, but the effect of spirulina on the small intestine epithelium is not well understood. Therefore, this study aims to investigate the proliferative effects of spirulina crude protein (SPCP) on a rat intestinal epithelial cells IEC-6 to elucidate the mechanisms underlying its effect. First, the results of wound-healing and cell viability assays demonstrated that SPCP promoted migration and proliferation in a dose-dependent manner. Subsequently, when the mechanisms of migration and proliferation promotion by SPCP were confirmed, we found that the epidermal growth factor receptor (EGFR) and mitogen-activated protein (MAPK) signaling pathways were activated by phosphorylation. Cell cycle progression from G0/G1 to S phase was also promoted by SPCP through upregulation of the expression levels of cyclins and cyclin-dependent kinases (Cdks), which regulate cell cycle progression to the S phase. Meanwhile, the expression of cyclin-dependent kinase inhibitors (CKIs), such as p21 and p27, decreased with SPCP. In conclusion, our results indicate that activation of EGFR and its downstream signaling pathway by SPCP treatment regulates cell cycle progression. Therefore, these results contribute to the research on the molecular mechanism for SPCP promoting the migration and proliferation of rat intestinal epithelial cells.

Etomidate Alleviates Ischemia-Anoxia Reperfusion Injury in Intestinal Epithelial Cells by Inhibiting the Activation of traf6-Regulated NF-KB Signaling

2022 ◽  
Vol 12 (5) ◽  
pp. 1015-1021
Author(s):  
Gen Lin ◽  
Ruichun Long ◽  
Xiaoqing Yang ◽  
Songsong Mao ◽  
Hongying Li
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Intestinal Epithelial Cells ◽  
Ischemia Reperfusion ◽  
Stress Factors ◽  
Inflammatory Factors ◽  
Intestinal Cell ◽  
Intestinal Epithelial

Objective: The present study aimed to investigate the role of etomidate in intestinal cell ischemia and hypoxia-reperfusion injury and potential mechanisms. Method: In this study, we establish the intestinal epithelial cells ischemia-reperfusion model in vitro. CCK8 was used to detect cell viability and flow cytometry assay was used to detect apoptosis levels of treated OGD/R model cells. ELISA measured the expression level of oxidative stress factors and inflammatory factors. Furthermore, western blot assay was used to detect the expression the apoptosis-related factors and TNFR-associated factors in treated OGD/R model cells. Result: Etomidate does not affect the activity of intestinal epithelial cells, and can protect intestinal epithelial cells to reduce ischemiareperfusion injury, and the expression of inflammatory factors and oxidative stress in cells with mild intestinal epithelial ischemia-reperfusion injury. Etomidate alleviates apoptosis of intestinal epithelial ischemia-reperfusion injury cells. Etomidate inhibits the activation of traf6-mediated NF-κB signal during ischemia-anoxia reperfusion of intestinal epithelial cells. Conclusion: Taken together, our study demonstrated that etomidate attenuates inflammatory response and apoptosis in intestinal epithelial cells during ischemic hypoxia-reperfusion injury and inhibits activation of NF-κB signaling regulated by TRAF6.

scholarly journals Comparative effect of bovine buttermilk, whey, and lactoferrin on the innate immunity receptors and oxidative status of intestinal epithelial cells.

2020 ◽  
Author(s):  
Berta Buey ◽  
Andrea Bellés ◽  
Eva Latorre ◽  
Inés Abad ◽  
María Dolores Pérez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Innate Immunity ◽  
Epithelial Cells ◽  
Milk Fat ◽  
Functional Foods ◽  
Intestinal Epithelial Cells ◽  
Protein Carbonyl ◽  
Intestinal Epithelial ◽  
Milk Fat Globule

Milk contains active molecules with important functional properties as the defensive proteins; among them are the whey protein lactoferrin and proteins of the milk fat globule membrane (MFGM) present in buttermilk. The aim of this study has been to investigate the effect of lactoferrin, whey and buttermilk as modulators of intestinal innate immunity and oxidative stress on intestinal epithelial cells, to evaluate its potential use for the development of functional foods. Innate immune Toll-like receptors (TLR2, TLR4, and TLR9) mRNA expression, lipid peroxidation (MDA+4-HDA) and protein carbonyl levels were analyzed in enterocyte-like Caco-2/TC7 cells treated for 24 hours with different concentrations of lactoferrin, whey or buttermilk. None of the substances analyzed caused oxidative damage; however, whey significantly decreased the levels of lipid peroxidation. Furthermore, both lactoferrin and whey were able to reduce the oxidative stress induced by lipopolysaccharide. Respect to TLR receptors, lactoferrin, whey and buttermilk specifically altered the expression of TLR2, TLR4 and TLR9 receptors, with a strong decrease in TLR4 expression. These results suggest that lactoferrin, whey and buttermilk could be interesting potential ingredients for functional foods as they seem to modulate oxidative stress and inflammatory response induced by TLRs activation.

Sign in / Sign up

Export Citation Format

Share Document