Eleutheroside B increase tight junction proteins and anti‐inflammatory cytokines expression in intestinal porcine jejunum epithelial cells (IPEC‐J2)

2019 ◽  
Author(s):  
Dongsheng Che ◽  
Bao Zhao ◽  
Yueli Fan ◽  
Rui Han ◽  
Chun Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Inflammatory Cytokines ◽  
Tight Junction Proteins ◽  
Eleutheroside B ◽  
Anti Inflammatory ◽  
Junction Proteins

scholarly journals Differential effects of claudin-3 and claudin-4 on alveolar epithelial barrier function

2011 ◽  
Vol 301 (1) ◽  
pp. L40-L49 ◽  
Author(s):  
Leslie A. Mitchell ◽  
Christian E. Overgaard ◽  
Christina Ward ◽  
Susan S. Margulies ◽  
Michael Koval
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Barrier Function ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial Cells ◽  
Epithelial Barrier ◽  
Tight Junction Proteins ◽  
Epithelial Barrier Function ◽  
Alveolar Epithelial ◽  
Junction Proteins

Alveolar barrier function depends critically on the claudin family tight junction proteins. Of the major claudins expressed by alveolar epithelial cells, claudin (Cldn)-3 and Cldn-4 are the most closely related by amino acid homology, yet they differ dramatically in the pattern of expression. Previously published reports have shown that Cldn-3 is predominantly expressed by type II alveolar epithelial cells; Cldn-4 is expressed throughout the alveolar epithelium and is specifically upregulated in response to acute lung injury. Using primary rat alveolar epithelial cells transduced with yellow fluorescent protein-tagged claudin constructs, we have identified roles for Cldn-3 and Cldn-4 in alveolar epithelial barrier function. Surprisingly, increasing expression of Cldn-3 decreased alveolar epithelial barrier function, as assessed by transepithelial resistance and dye flux measurements. Conversely, increasing Cldn-4 expression improved alveolar epithelial transepithelial resistance compared with control cells. Other alveolar epithelial tight junction proteins were largely unaffected by increased expression of Cldn-3 and Cldn-4. Taken together, these results demonstrate that, in the context of the alveolar epithelium, Cldn-3 and Cldn-4 have different effects on paracellular permeability, despite significant homology in their extracellular loop domains.

scholarly journals The Role of β-Carotene in Colonic Inflammation and Intestinal Barrier Integrity

2021 ◽  
Vol 8 ◽  
Author(s):  
Junrui Cheng ◽  
Emilio Balbuena ◽  
Baxter Miller ◽  
Abdulkerim Eroglu
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Signaling Pathway ◽  
Tight Junction Proteins ◽  
Colonic Epithelial Cells ◽  
Colonic Inflammation ◽  
Tlr4 Signaling Pathway ◽  
Β Carotene ◽  
Junction Proteins

Background: Carotenoids are naturally occurring pigments accounting for the brilliant colors of fruits and vegetables. They may display antioxidant and anti-inflammatory properties in humans besides being precursors to vitamin A. There is a gap of knowledge in examining their role within colonic epithelial cells. We proposed to address this research gap by examining the effects of a major dietary carotenoid, β-carotene, in the in vitro epithelial cell model.Methods: We examined the function of β-carotene in the lipopolysaccharide (LPS)/toll-like receptor 4 (TLR4) signaling pathway. We conducted western blotting assays to evaluate expressions of TLR4 and its co-receptor, CD14. We also examined NF-κB p65 subunit protein levels in the model system. Furthermore, we studied the impact of β-carotene on the tight junction proteins, claudin-1, and occludin. We further carried out immunocytochemistry experiments to detect and visualize claudin-1 expression.Results: β-Carotene reduced LPS-induced intestinal inflammation in colonic epithelial cells. β-Carotene also promoted the levels of tight junction proteins, which might lead to enhanced barrier function.Conclusions: β-Carotene could play a role in modulating the LPS-induced TLR4 signaling pathway and in enhancing tight junction proteins. The findings will shed light on the role of β-carotene in colonic inflammation and also potentially in metabolic disorders since higher levels of LPS might induce features of metabolic diseases.

scholarly journals Eucalyptol Blocks Diabetes-Associated Disruption of Tight Junction and Blood Retinal Barrier in Retinal Pigment Epithelial Cells and Diabetic Eyes

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 413-413
Author(s):  
Dongyeon Kim ◽  
Min-kyung Kang ◽  
Young-Hee Kang
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelial Cells ◽  
Tight Junction Proteins ◽  
Blood Retinal Barrier ◽  
Pigment Epithelial ◽  
Pigment Epithelial Cells ◽  
Junction Proteins

Abstract Objectives Diabetes-associated retinal impairment has been implicated in diabetic retinopathy. Chronic hyperglycemia leads to disruption of tight junction and breakdown of blood retinal barrier. Eucalyptol is a natural organic essential oil and a monoterpenoid present in eucalyptus oil with anti-inflammatory, anti-diabetic and antioxidant properties. Methods Primary human retinal pigment epithelial cells (HRPEC) were cultured in media containing 33 mM glucose for 4 days in the presence of 1–20 μM eucalyptol. The in vivo animal study employed db/db mice orally administrated with 10 mg/kg eucalyptol. Cell lysates and mouse eye tissue extracts were prepared for Western blotting, in which antibodies of ZO-1, occludin, matrix metalloproteinase (MMP)-2 and MMP-9 were used. Results Eucalyptol enhanced epithelial induction of the tight junction proteins of ZO-1 and occludin reduced by glucose loading. Consistently, oral administration of eucalyptol to db/db mice augmented the eye tissue levels of these tight junction proteins. In addition, the induction of MMP-2 and MMP-9 involved in the degradation of extracellular matrix, was elevated by exposure of glucose to HRPEC, which was encumbered by eucalyptol in a dose-dependent manner. Conclusions These results demonstrated that eucalyptol maintained transepithelial cells integrity and blood retinal barrier in diabetic eyes. Therefore, eucalyptol may be a potent retinoprotective agent combating diabetes-associated retinal malfunction. Funding Sources This work was supported by the National Research Foundation of Korea (NRF) grants funded by the Korea government (2017R1A6A3A04011473).

Alanyl-glutamine ameliorates lipopolysaccharide-induced inflammation and barrier function injury in bovine jejunum epithelial cells

2019 ◽  
Vol 97 (6) ◽  
pp. 670-680 ◽  
Author(s):  
Xianglun Zhang ◽  
Xiuwen Tan ◽  
Yifan Liu ◽  
Wei You ◽  
Guifen Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Tight Junction ◽  
Cell Viability ◽  
Barrier Function ◽  
Intestinal Inflammation ◽  
Inflammatory Factors ◽  
Tight Junction Proteins ◽  
Mrna And Protein Expression ◽  
Junction Proteins

The aim of this study was to investigate the effects of alanyl-glutamine (Ala-Gln) on the regulation of lipopolysaccharide (LPS)-induced inflammation and barrier function in bovine jejunum epithelial cells (BJECs). BJECs were exposed (or not) to 1 μg/mL LPS for 24 h to generate a pro-inflammatory model. The cells were then treated with different concentrations of Ala-Gln (0.25, 0.5, 1.0, 2.0, or 4.0 mmol/L) to detect any regulatory effects on the inflammation and barrier function of BJECs. LPS decreased cell viability and enhanced the production of the pro-inflammatory cytokines interleukin (IL)-6 and IL-8. LPS induced inflammation and damaged the barrier function of BJECs, as evidenced by up-regulated mRNA and protein expression of inflammatory factors and down-regulated expression of tight junction proteins. Conversely, Ala-Gln rescued the decrease in cell viability and prevented the accumulation of ILs after LPS exposure by reducing the mRNA and protein expression levels of inflammatory factors. In addition, Ala-Gln induced the mRNA and protein expression of multiple tight junction proteins, and thus reconstituted the barrier function of BJECs. In conclusion, Ala-Gln attenuates injury from inflammation and repairs damaged intestinal barrier induced with LPS, suggesting its potential as a therapeutic agent against intestinal inflammation in mammals.

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