Nanoparticles derived from porcine bone soup attenuate oxidative stress-induced intestinal barrier injury in Caco-2 cell monolayer model

Gelsemium elegans Benth. (G. elegans), a traditional Chinese medicine, has great potential as an effective growth promoter in animals, however, the mechanism of its actin remains unclear. Here, we evaluated the protective effects of koumine extract from G. elegans against lipopolysaccharide (LPS)-induced intestinal barrier dysfunction in IPEC-J2 cells through alleviation of inflammation and oxidative stress. MTT and LDH assays revealed that koumine significantly reduced LPS cytotoxicity. Transepithelial electrical resistance (TEER) and cell monolayer permeability assays showed that koumine treatment attenuated the LPS-induced intestinal barrier dysfunction with no particularly different effects in tight junction proteins such as ZO-1, claudin-1, and occludin. LPS-triggered inflammatory response was also suppressed by koumine, as evidenced by the downregulated inflammatory factors, including TNF-[Formula: see text], IL-6, IL-1[Formula: see text], NO, iNOS, and COX-2, which was closely connected with the inhibition of NF-[Formula: see text]B pathway for the decrease of phosphorylation of I[Formula: see text]B[Formula: see text] and NF-[Formula: see text]B and nuclear translocation of p-p65. Amount of reactive oxygen species (ROS) and MDA induced by LPS was also reduced by koumine through activation of Nrf2 pathway, and increased in the levels of Nrf2 and HO-1 degradation of keap-1 to promote anti-oxidants, including superoxide dismutase (SOD) and catalase (CAT). To summarize, koumine-reduced the oxidative stress and inflammatory reaction triggered by LPS through regulation of the Nrf2/NF-[Formula: see text]B signaling pathway and preventing intestinal barrier dysfunction.

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Mo1929 – Candida Albicans Sc5314 Inhibits Nlrp3/Nlrp6 Inflammasome Expression and Dampens Human Intestinal Barrier Activity in Caco-2 Cell Monolayer Model

Gastroenterology ◽

10.1016/s0016-5085(19)39196-6 ◽

2019 ◽

Vol 156 (6) ◽

pp. S-890

Author(s):

Xiaqiong Mao ◽

Hongjie Zhang ◽

Xinyun Qiu ◽

Chunhua Jiao

Keyword(s):

Candida Albicans ◽

Cell Monolayer ◽

Intestinal Barrier ◽

Monolayer Model

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Dietary l-tryptophan alleviated LPS-induced intestinal barrier injury by regulating tight junctions in a Caco-2 cell monolayer model

Food & Function ◽

10.1039/c9fo00123a ◽

2019 ◽

Vol 10 (5) ◽

pp. 2390-2398 ◽

Cited By ~ 3

Author(s):

Mengdie Chen ◽

Yuyu Liu ◽

Shanbai Xiong ◽

Moucheng Wu ◽

Bin Li ◽

...

Keyword(s):

Tight Junctions ◽

Cell Monolayer ◽

Intestinal Barrier ◽

Intestinal Epithelial ◽

Epithelial Layer ◽

Infection And Inflammation ◽

Monolayer Model ◽

Cell Cell

The intestinal epithelial layer forms a barrier through cell–cell tight junctions and breaking or even slightly disrupting this barrier can lead to serious pathological consequences, including infection and inflammation.

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Inhibition of p38 Mitogen-Activated Protein Kinase Attenuates Butyrate-Induced Intestinal Barrier Impairment in a Caco-2 Cell Monolayer Model

Journal of Pediatric Gastroenterology and Nutrition ◽

10.1097/mpg.0000000000000369 ◽

2014 ◽

Vol 59 (2) ◽

pp. 264-269 ◽

Cited By ~ 11

Author(s):

Xiao-Zhong Huang ◽

Zhong-Rong Li ◽

Li-Bin Zhu ◽

Hui-Ya Huang ◽

Long-Long Hou ◽

...

Keyword(s):

Protein Kinase ◽

Cell Monolayer ◽

Intestinal Barrier ◽

Mitogen Activated Protein Kinase ◽

Mitogen Activated Protein ◽

Monolayer Model

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The Protective Effects of Orthosiphon stamineus Extract Against Intestinal Barrier Injury in High-Fat Diet-Induced Mouse and Oxidative Stress Cell Models

Natural Product Communications ◽

10.1177/1934578x20985346 ◽

2021 ◽

Vol 16 (1) ◽

pp. 1934578X2098534

Author(s):

Xuan Cai ◽

Lihui Zhu ◽

Xiaofeng Yin ◽

Huiqin Xue ◽

Changfeng Xiao ◽

...

Keyword(s):

Oxidative Stress ◽

High Fat Diet ◽

Cell Model ◽

Kidney Diseases ◽

Cell Monolayer ◽

Intestinal Barrier ◽

Intestinal Barrier Function ◽

Protective Effects ◽

High Fat ◽

Orthosiphon Stamineus

Orthosiphon stamineus Benth. (Lamiaceae) is commonly used for the treatment of kidney diseases, but its role in intestinal barrier function remains unknown. The present study investigated the protective effects of O. stamineus extract (OE) against oxidative stress-induced injury to the small intestinal epithelium and the possible mechanism. High-performance liquid chromatography fingerprinting was used to analyze OE. Oxidative stress was induced by hydrogen peroxide (1 mM for 1 hour) in an IPEC-J2 cell monolayer model and a high-fat diet in C57BL/6 mice (8 weeks). The malondialdehyde (MDA) content was tested in both models. To evaluate permeability, transepithelial electrical resistance (TEER) was tested in a cell model. Serum diamine oxidase (DAO) and endotoxin contents were determined in a mouse model, and histological sections were analyzed. The messenger ribonucleic acid expression of tight junction proteins was measured by quantitative real-time polymerase chain reaction. Pretreatment with OE (50 µg/mL) increased the IPEC-J2 cell monolayer TEER (12.4%) and decreased MDA (from 6.1 to 4.7 mmol/mg prot). Oral administration of OE (100 mg/kg) decreased serum DAO (34.2%), endotoxin (13.4%), and MDA (from 21.3 to 11.0 mmol/mL) in mice. OE upregulated ZO-1 (42.8% in the cell model and 125.0% in mice) and occluding (127.0% in the cell model and 120.3% in mice) gene expression. These results confirmed the protective effect of OE on the intestinal barrier, which was associated with the antioxidant effect of OE; thus, OE is suitable for the prevention and treatment of intestinal barrier injury.

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Protective Role of Natural and Semi-Synthetic Tocopherols on TNFα-Induced ROS Production and ICAM-1 and Cl-2 Expression in HT29 Intestinal Epithelial Cells

Antioxidants ◽

10.3390/antiox10020160 ◽

2021 ◽

Vol 10 (2) ◽

pp. 160

Author(s):

Vladana Domazetovic ◽

Irene Falsetti ◽

Caterina Viglianisi ◽

Kristian Vasa ◽

Cinzia Aurilia ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Properties ◽

Intestinal Barrier ◽

Protective Role ◽

Intercellular Adhesion Molecule ◽

Intestinal Epithelial ◽

Intercellular Adhesion Molecule 1 ◽

Beneficial Effects ◽

Bowel Diseases

Vitamin E, a fat-soluble compound, possesses both antioxidant and non-antioxidant properties. In this study we evaluated, in intestinal HT29 cells, the role of natural tocopherols, α-Toc and δ-Toc, and two semi-synthetic derivatives, namely bis-δ-Toc sulfide (δ-Toc)2S and bis-δ-Toc disulfide (δ-Toc)2S2, on TNFα-induced oxidative stress, and intercellular adhesion molecule-1 (ICAM-1) and claudin-2 (Cl-2) expression. The role of tocopherols was compared to that of N-acetylcysteine (NAC), an antioxidant precursor of glutathione synthesis. The results show that all tocopherol containing derivatives used, prevented TNFα-induced oxidative stress and the increase of ICAM-1 and Cl-2 expression, and that (δ-Toc)2S and (δ-Toc)2S2 are more effective than δ-Toc and α-Toc. The beneficial effects demonstrated were due to tocopherol antioxidant properties, but suppression of TNFα-induced Cl-2 expression seems not only to be related with antioxidant ability. Indeed, while ICAM-1 expression is strongly related to the intracellular redox state, Cl-2 expression is TNFα-up-regulated by both redox and non-redox dependent mechanisms. Since ICAM-1 and Cl-2 increase intestinal bowel diseases, and cause excessive recruitment of immune cells and alteration of the intestinal barrier, natural and, above all, semi-synthetic tocopherols may have a potential role as a therapeutic support against intestinal chronic inflammation, in which TNFα represents an important proinflammatory mediator.

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Regulatory effects of flavonoids luteolin on BDE-209-induced intestinal epithelial barrier damage in Caco-2 cell monolayer model

Food and Chemical Toxicology ◽

10.1016/j.fct.2021.112098 ◽

2021 ◽

Vol 150 ◽

pp. 112098

Author(s):

Jinwen Yuan ◽

Siyan Che ◽

Zheng Ruan ◽

Luqing Song ◽

Rongxue Tang ◽

...

Keyword(s):

Cell Monolayer ◽

Epithelial Barrier ◽

Intestinal Epithelial ◽

Intestinal Epithelial Barrier ◽

Regulatory Effects ◽

Monolayer Model ◽

Bde 209

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Cystine reduces tight junction permeability and intestinal inflammation induced by oxidative stress in Caco-2 cells

Amino Acids ◽

10.1007/s00726-021-03001-y ◽

2021 ◽

Author(s):

Tatsuya Hasegawa ◽

Ami Mizugaki ◽

Yoshiko Inoue ◽

Hiroyuki Kato ◽

Hitoshi Murakami

Keyword(s):

Oxidative Stress ◽

Tight Junction ◽

Mrna Expression ◽

Inflammatory Cytokines ◽

Inflammatory Responses ◽

Intestinal Barrier ◽

Barrier Dysfunction ◽

Whole Cells ◽

Intestinal Barrier Dysfunction ◽

Pro Inflammatory Cytokines

AbstractIntestinal oxidative stress produces pro-inflammatory cytokines, which increase tight junction (TJ) permeability, leading to intestinal and systemic inflammation. Cystine (Cys2) is a substrate of glutathione (GSH) and inhibits inflammation, however, it is unclear whether Cys2 locally improves intestinal barrier dysfunction. Thus, we investigated the local effects of Cys2 on oxidative stress-induced TJ permeability and intestinal inflammatory responses. Caco-2 cells were cultured in a Cys2-supplemented medium for 24 h and then treated with H2O2 for 2 h. We assessed TJ permeability by measuring transepithelial electrical resistance and the paracellular flux of fluorescein isothiocyanate–dextran 4 kDa. We measured the concentration of Cys2 and GSH after Cys2 pretreatment. The mRNA expression of pro-inflammatory cytokines was assessed. In addition, the levels of TJ proteins were assessed by measuring the expression of TJ proteins in the whole cells and the ratio of TJ proteins in the detergent-insoluble fractions to soluble fractions (IS/S ratio). Cys2 treatment reduced H2O2-induced TJ permeability. Cys2 did not change the expression of TJ proteins in the whole cells, however, suppressed the IS/S ratio of claudin-4. Intercellular levels of Cys2 and GSH significantly increased in cells treated with Cys2. Cys2 treatment suppressed the mRNA expression of pro-inflammatory cytokines, and the mRNA levels were significantly correlated with TJ permeability. In conclusion, Cys2 treatment locally reduced oxidative stress-induced intestinal barrier dysfunction possively due to the mitigation of claudin-4 dislocalization. Furthermore, the effect of Cys2 on the improvement of intestinal barrier function is related to the local suppression of oxidative stress-induced pro-inflammatory responses.

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