Cyanidin-3- O -glucoside inhibits NF-kB signalling in intestinal epithelial cells exposed to TNF-α and exerts protective effects via Nrf2 pathway activation

2016 ◽  
Vol 264 ◽  
pp. 51-58 ◽  
Author(s):  
Daniela Ferrari ◽  
Antonio Speciale ◽  
Mariateresa Cristani ◽  
Deborah Fratantonio ◽  
Maria Sofia Molonia ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Protective Effects ◽  
Intestinal Epithelial ◽  
Nrf2 Pathway ◽  
Pathway Activation ◽  
Tnf Α

Protective effects of baicalin on LPS-induced injury in intestinal epithelial cells and intercellular tight junctions

2015 ◽  
Vol 93 (4) ◽  
pp. 233-237 ◽  
Author(s):  
Jian Chen ◽  
Ren Zhang ◽  
Jian Wang ◽  
Peng Yu ◽  
Quan Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Tight Junctions ◽  
Inflammatory Cytokines ◽  
Intestinal Epithelial Cells ◽  
Expression Level ◽  
Protective Effects ◽  
Intestinal Epithelial ◽  
Tnf Α ◽  
Mrna And Protein Expression

Aims: To investigate the protective effects and mechanisms of baicalin on lipopolysaccharide (LPS)-induced injury in intestinal epithelial cells and intercellular tight junctions. Methods: IEC-6 cells were stimulated with LPS (1.0 μg/mL), with or without baicalin, for 24 h. The levels of the inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α were determined using ELISA. Quantitative real-time PCR was used for determining the mRNA expression level of claudin-3, occludin, and ZO-1; Western blot and immunofluorescence analysis were used for analyzing the expression level and the distribution patterns of ZO-1 protein. Results: Pretreatment with baicalin (10.0 μg/mL) improved LPS-stimulated cell viability and repressed IL-6 and TNF-α levels. In addition, pretreatment with baicalin up-regulated mRNA and protein expression levels of ZO-1 and kept the protein intact in IEC-6 cells injured with LPS. Conclusion: Baicalin has the capacity to protect IEC-6 cells and the intercellular tight junctions from LPS-induced injury. The mechanisms may be associated with inhibiting the production of inflammatory cytokines, and up-regulating the mRNA and protein expression of ZO-1.

scholarly journals Effect of berberine on LPS-induced expression of NF-κB/MAPK signalling pathway and related inflammatory cytokines in porcine intestinal epithelial cells

2020 ◽  
Vol 26 (7) ◽  
pp. 627-634 ◽  
Author(s):  
Zhang Zhu ◽  
Li Xueying ◽  
Li Chunlin ◽  
Xiong Wen ◽  
Zeng Rongrong ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Signalling Pathway ◽  
Inflammatory Factors ◽  
Mrna Levels ◽  
Protective Effects ◽  
Intestinal Epithelial ◽  
Mapk Signalling Pathway ◽  
Tnf Α ◽  
Mapk Signalling

Berberine is an alkaloid extracted from medicinal plants such as Coptis chinensis and Phellodendron chinense. It possesses anti-inflammatory, anti-tumour and anti-oxidation properties, and regulates Glc and lipid metabolism. This study explored the mechanisms of the protective effects of berberine on barrier function and inflammatory damage in porcine intestinal epithelial cells (IPEC-J2) induced by LPS. We first evaluated the effects of berberine and LPS on cell viability. IPEC-J2 cells were treated with 5 μg/ml LPS for 1 h to establish an inflammatory model, and 75, 150 and 250 μg/ml berberine were used in further experiments. The expression of IL-1β, IL-6 and TNF-α was measured by RT-PCR. The key proteins of the NF-κB/MAPK signalling pathway (IκBα, p-IκBα, p65, p-p65, c-Jun N-terminal kinase (JNK), p-JNK, p38, p-p38, ERK1/2 and p-ERK1/2) were detected by Western blot. Upon exposure to LPS, IL-1β, IL-6 and TNF-α mRNA levels and p-IκBα p-p65 protein levels were significantly enhanced. Pre-treatment with berberine reduced the expression of inflammatory factors and was positively correlated with its concentration, and dose dependently inhibited the expression of IκBα, p-IκBα, p-p65, p-p38 and JNK. These results demonstrated that pre-treating intestinal epithelial cells with berberine was useful in preventing and treating diarrhoea induced by Escherichia coli in weaned pigs.

Glutamine protects intestinal epithelial cells: role of inducible HSP70

1997 ◽  
Vol 272 (4) ◽  
pp. G879-G884 ◽  
Author(s):  
P. E. Wischmeyer ◽  
M. W. Musch ◽  
M. B. Madonna ◽  
R. Thisted ◽  
E. B. Chang
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Mucosal Healing ◽  
Epithelial Cell Line ◽  
Protective Effects ◽  
Intestinal Epithelial ◽  
Cellular Protection ◽  
Gut Mucosa ◽  
Shock Proteins ◽  
Hsp70 Induction

Glutamine (Gln) protects gut mucosa against injury and promotes mucosal healing. Because the induction of heat shock proteins (HSP) protects cells under conditions of stress, we determined whether Gln conferred protection against stress in an intestinal epithelial cell line through HSP induction. Gln added to IEC-18 cells induces an increase in HSP70, a concentration-dependent effect also seen with mRNA. Two forms of injury, lethal heat (49 degrees C) and oxidant, were used, and viability was determined by 51Cr release. Gln-treated cells were significantly more resistant to injury. Treatment with 6-diazo-5-oxo-L-norleucine (DON), a nonmetabolizable analog of Gln, induced HSP70 and protected cells from injury, but less than Gln. These findings suggest that the effects of Gln on HSP70 induction and cellular protection are mediated by metabolic and nonmetabolic mechanisms. To determine whether HSP induction was central to the action of Gln and DON, quercetin, which blocks HSP induction, was used. Quercetin blocked HSP70 induction and the protective effect of Gln and DON. We conclude that the protective effects of Gln in intestinal epithelial cells are in part mediated by HSP70 induction.

scholarly journals Intestinal Epithelial Cells With Impaired Autophagy Lose Their Adhesive Capacity in the Presence of TNF-α

2011 ◽  
Vol 140 (5) ◽  
pp. S-84
Author(s):  
Masaya Saito ◽  
Tomoo Nakagawa ◽  
Yoshiko Noguchi ◽  
Toru Sato ◽  
Tatsuro Katsuno ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Tnf Α ◽  
Adhesive Capacity

Proinflammatory cytokines TNF-α and IFN-γ alter laminin expression under an apoptosis-independent mechanism in human intestinal epithelial cells

2004 ◽  
Vol 287 (3) ◽  
pp. G592-G598 ◽  
Author(s):  
Caroline Francoeur ◽  
Fabrice Escaffit ◽  
Pierre H. Vachon ◽  
Jean-François Beaulieu
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Proinflammatory Cytokines ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Laminin 5 ◽  
Cell Functions ◽  
Tnf Α ◽  
Independent Mechanism ◽  
Ifn Γ

Laminins are basement membrane molecules that mediate cell functions such as adhesion, proliferation, migration, and differentiation. In the normal small intestine, laminin-5 and -10 are mainly expressed at the base of villus cells. However, in Crohn's disease (CD), a major redistribution of these laminins to the crypt region of the inflamed ileal mucosa has been observed, suggesting a possible relationship between laminin expression and cytokine and/or growth factor production, which is also altered in CD. The aim of this study was to test the hypothesis that proinflammatory cytokines can modulate laminin expression by intestinal epithelial cells. The effect of TNF-α, IFN-γ, IL-1β, IL-6, and transforming growth factor (TGF)-β was analyzed on the expression of laminins in the normal human intestinal epithelial crypt (HIEC) cell line. When treated with a single cytokine, HIEC cells secreted small amounts of laminin-5 and -10. Only TNF-α and TGF-β induced a slight increase in the secretion of these laminins. However, in combination, TNF-α and IFN-γ synergistically stimulated the secretion of both laminin-5 and -10 in HIEC cells. Transcript analyses suggested that the upregulation of the two laminins might depend on distinct mechanisms. Interestingly, the TNF-α and IFN-γ combination was also found to significantly promote apoptosis. However, the effect of cytokines on the secretion of laminins was maintained even after completely blocking apoptosis by inhibiting caspase activities. These results demonstrate that laminin production is specifically modulated by the proinflammatory cytokines TNF-α and IFN-γ in intestinal epithelial cells under an apoptosis-independent mechanism.

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