Vitamin A inhibits the action of LPS on the intestinal epithelial barrier function and tight junction proteins

He, Caimei; Deng, Jun; Hu, Xin; Zhou, Sichun; Wu, Jingtao; Xiao, Di; Darko, Kwame Oteng; Huang, Yanjun; Tao, Ting; Peng, Mei; Wang, Zhiren; Yang, Xiao‐Ping

doi:10.1039/c8fo01123k

Cited by 143 publications

(108 citation statements)

References 28 publications

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“…Studies have confirmed that LPS, one commonly and important inflammation activator, produces damages on tight junctions in vitro (Chen et al, ; Main, Weber, Baumgard, & Gabler, ). Previously, we have shown that VA protected against LPS‐induced damage on tight junctions in vitro (He et al, ). However, whether or how effect of VA on tight junction of intestine in vivo remains elusive.…”

Section: Introductionmentioning

confidence: 81%

“…Recently, it has been reported that the development of inflammation ‐caused diseases is associated with alteration of intestinal tissue proteins, particularly tight junction proteins (Yang et al, ). Our previous study has shown that VA inhibits the action of LPS on the intestinal epithelial barrier function and tight junction proteins at cellular level (He et al, ). However, it is unknown whether this protective effect of VA could be seen in vivo or not.…”

Section: Discussionmentioning

confidence: 99%

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Vitamin A prevents lipopolysaccharide‐induced injury on tight junctions in mice

Xiao

et al. 2020

Food Science & Nutrition

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Vitamin A (VA) is one of the most widely used food supplements, but its molecular mechanisms largely remain elusive. Previously, we have demonstrated that VA inhibits the action of lipopolysaccharide (LPS) on intestinal epithelial barrier function and tight junction proteins using IPEC‐J2 cells, one of representative intestinal cell lines as a cellular model. These exciting findings stimulated us continue to determine the effects of VA on LPS‐induced damage of intestinal integrity in mice. Our results demonstrated that LPS treatment caused reductions of the mRNA levels of tight junction proteins including Zo‐1, Occludin, and Claudin‐1, well‐known biomarkers of intestinal integrity, and these reductions were reversed by VA pretreatment. Intestinal immunofluorescent results of Claudin‐1 revealed that LPS disrupted the structure of tight junction and reduced the expression of Claudin‐1 at protein level, which was reversed by VA pretreatment. These results suggest that VA may exert a profound role on preventing intestinal inflammation in vivo.

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Section: Introductionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Vitamin A prevents lipopolysaccharide‐induced injury on tight junctions in mice

Xiao

et al. 2020

Food Science & Nutrition

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“…TJs can be compromised by luminal noxious antigens, one of which is lipopolysaccharides (LPS), the main component of the outer membrane of Gram-negative bacteria. Growing investigations indicate that LPS triggers an inflammatory signaling cascade to reduce tight junction protein expression, leading to increased intestinal permeability and disrupting intestinal epithelial barrier function (He et al, 2019;Tunisi et al, 2019). Clinical study also demonstrated that circulating blood LPS levels are elevated in Crohn's disease and sepsis patients, and contribute to the pathogenesis of intestinal and systemic inflammatory response (Guo et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Ferulic Acid Ameliorates Lipopolysaccharide-Induced Barrier Dysfunction via MicroRNA-200c-3p-Mediated Activation of PI3K/AKT Pathway in Caco-2 Cells

Guo

Zhao

et al. 2020

Front. Pharmacol.

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Intestinal barrier dysfunction is an important clinical problem in various acute and chronic pathological conditions. Ferulic acid (FA) can attenuate the intestinal epithelial barrier dysfunction, however, the underlying mechanism remains unclear. The present study aimed to uncover the protective effect of FA on intestinal epithelial barrier dysfunction in a Caco-2 cell model of lipopolysaccharide (LPS) stimulation and the underlying mechanism. Caco-2 cells were pretreated with FA and then exposed to LPS stimulation. The barrier function of Caco-2 cells was evaluated by measuring trans-epithelial resistance (TER) and 4-kDa fluorescein isothiocyanate (FITC)-dextran (FD4) flux, and analyzing the tight junction protein expression and structure. The results showed that decreased TER and increased FITC-FD4 flux were observed in Caco-2 cells stimulated with LPS, but these effects were attenuated by FA pretreatment. FA pretreatment inhibited LPS-induced decrease in occludin and ZO-1 mRNA and protein expression. LPS stimulation decreased miR-200c-3p expression, whereas this decrease was inhibited by FA pretreatment. Furthermore, overexpression of miR-200c-3p strengthened the protective effects of FA on LPS-induced Caco-2 cell barrier dysfunction by decreasing epithelial permeability, increasing occludin and ZO-1 protein expression, and maintaining of ZO-1 protein distribution, while suppression of miR-200c-3p reversed the protective effects of FA. LPS treatment increased the expression of PTEN protein and decreased expression of phosphorylated PI3K and AKT proteins. However, pretreatment of FA inhibited expression of PTEN protein and promoted activation of PI3K/AKT signaling pathway in the LPS-treated Caco-2 cells, and this regulatory effect of FA on the PTEN/PI3K/AKT signaling pathway was strengthened or weakened by miR-200c-3p overexpression or suppression, respectively. Our findings suggested that in Caco-2 cells, FA promotes activation of PI3K/AKT pathway by miR-200c-3p-mediated suppression of the negative

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“…A previous study showed that β-carotene can promote gap junctional intercellular communication [15]. Another study also demonstrated that Vitamin A recovered LPS-induced in ammation-mediated intestinal barrier dysfunction and re-boosted LPS-induced decreases of ZO-1, Occludin and Claudin-1 at the tight junctions in IPEC-J2 cells [36]. Therefore, these data suggest that β-carotene increases TJ protein expression and improves epithelial barrier function in the intestine.…”

Section: Discussionmentioning

confidence: 63%

Dietary Supplementation of β-Carotene on Growth Performance, Jejunal Permeability and Tight Junction Proteins in Weaned piglets

Lang¹,

Gong

et al. 2020

Preprint

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Background: Weaning causes stress syndrome in the newborns, while it can lead to many intestinal diseases. The aim of this study was to determine the dietary supplementation of β-carotene on growth performance, jejunal permeability and tight junction proteins in weaned piglets, and explore the underlying mechanisms by which β-carotene regulates tight junction proteins. The positive control group was fed sow's milk throughout the trial. The negative control group was weaned at d 21 without any supplementation. Two experimental groups of piglets were weaned at d 21 and fed 40 mg/kg or 80 mg/kg β-carotene-supplemented diets from d 14 to d 24, respectively. Blood and the jejunum were collected at d 24. Results: The results showed that β-carotene at 80 mg/kg increased initial and final body weight and average daily feed intake, improved the villus height at d 24 (p<0.05) but reduced crypt depth in weaned piglets at d 24 (p<0.05). Additionally, β-carotene protected intestinal morphology. Supplemental 80 mg/kg β-carotene reduced the concentrations of D-lactic acid and diamine oxidase in serum (p<0.05) but enhanced the mRNA expression of claudin-3, occludin (p<0.05), and zonula occludens protein-1(p>0.05) and the protein levels of claudin-3 (p<0.01), occludin (p<0.05), and zonula occludens protein-1 (p>0.05) in the jejunum at d 24. Using intestinal epithelial cells and a Rac1 inhibitor in vitro, we demonstrated that the β-carotene-induced higher tight junction proteins might depend on the Rac1 pathway. Conclusions: β-carotene improved growth performance and attenuated jejunal permeability and tight junction proteins in weaned piglets, suggesting that β-carotene at 80 mg/kg may be an effective way for keeping healthier intestine of weaning piglets due to weaning.

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Vitamin A inhibits the action of LPS on the intestinal epithelial barrier function and tight junction proteins

Abstract: Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases.

Cited by 143 publications

References 28 publications

Vitamin A prevents lipopolysaccharide‐induced injury on tight junctions in mice

Vitamin A prevents lipopolysaccharide‐induced injury on tight junctions in mice

Ferulic Acid Ameliorates Lipopolysaccharide-Induced Barrier Dysfunction via MicroRNA-200c-3p-Mediated Activation of PI3K/AKT Pathway in Caco-2 Cells

Dietary Supplementation of β-Carotene on Growth Performance, Jejunal Permeability and Tight Junction Proteins in Weaned piglets

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