Vitamin A supplementation improves the intestinal mucosal barrier and facilitates the expression of tight junction proteins in rats with diarrhea

Nutrition ◽  
2019 ◽  
Vol 57 ◽  
pp. 97-108 ◽  
Author(s):  
Lu Xiao ◽  
Ting Cui ◽  
Shu Liu ◽  
Baolin Chen ◽  
Yuting Wang ◽  
...  
2018 ◽  
Vol 20 (1) ◽  
pp. 20 ◽  
Author(s):  
Haiwei Liang ◽  
Zhaolai Dai ◽  
Jiao Kou ◽  
Kaiji Sun ◽  
Jingqing Chen ◽  
...  

l-Tryptophan (Trp) is known to play an important role in the health of the large intestine. However, a role of dietary Trp in the small-intestinal mucosal barrier and microbiota remains poorly understood. The present study was conducted with weaned piglets to address this issue. Postweaning piglets were fed for 4 weeks a corn- and soybean meal-based diet supplemented with 0 (Control), 0.1, 0.2, or 0.4% Trp. The small-intestinal microbiota and serum amino acids were analyzed by bacterial 16S rRNA gene-based high-throughput sequencing methods and high-performance liquid chromatography, respectively. The mRNA levels for genes involved in host defense and the abundances of tight-junction proteins in jejunum and duodenum were measured by real time-PCR and Western blot techniques, respectively. The concentrations of Trp in the serum of Trp-supplemented piglets increased in a dose-dependent manner. Compared with the control group, dietary supplementation with 0.2–0.4% Trp reduced the abundances of Clostridium sensu stricto and Streptococcus in the jejunum, increased the abundances of Lactobacillus and Clostridium XI (two species of bacteria that can metabolize Trp) in the jejunum, and augmented the concentrations of secretory immunoglobulin A (sIgA) as well as mRNA levels for porcine β-defensins 2 and 3 in jejunal tissues. Moreover, dietary Trp supplementation activated the mammalian target of rapamycin signaling and increased the abundances of tight-junction proteins (zonula occludens (ZO)-1, ZO-3, and claudin-1) in jejunum and duodenum. We suggested that Trp-metabolizing bacteria in the small intestine of weaned pigs primarily mediated the beneficial effects of dietary Trp on its mucosal integrity, health, and function.


2019 ◽  
Author(s):  
Fubin Qiu ◽  
Zehui Zhang ◽  
Ying Ma ◽  
Linxue Yang ◽  
Rui Li

Abstract Background: Tight junction proteins play crucial role in maintaining the intestinal mucosal barrier. Although previous studies had shown that the Notch signal is closely related to tight junction proteins, the mechanism by which it does so remains unknown. The goal of the present study was to investigate whether vitamin C combined with vitamin D3 affects intestinal mucosal barrier stability through Notch signal pathway.Results: To assess the effect of vitamin C combined with vitamin D3 on the intestinal mucosal barrier, electron microscopic observation of ultrastructure of tight junctions was done. And tight junction proteins gene and Notch signal gene expression were analyzed by quantitative reverse-transcription polymerase chain reaction, expression of tight junction protein in SW480 cells interfered with by LPS were examined by western blot. We found that vitamin C combined with vitamin D3 had protective effect on DSS-induced ulcerative colitis in guinea pig intestinal mucosa. Electron microscopy results showed that both low dose and high dose of vitamin C combined with vitamin D3 could maintain DSS-induced ulcerative colitis in guinea pig intestinal epithelium tight junction, however, the combination of medium dose vitamin C and vitamin D3 did not have this effect; Compared with the control group, the expression level of ZO-1 mRNA in the colon tissue of high-dose vitamin C group was significantly increased. In SW480 cell experiments, compared with the control group, the cell migration and repair ability of different concentrations of vitamin C combined with vitamin D3 group were significantly improved, the protein expression of Notch-1 was increased, but the protein expression of claudin-2 was significantly decreased. Conclusions: our results of this experiment showed that the appropriate amount of vitamin C combined with vitamin D3 might regulate the expression of claudin-2 by regulating Notch-1, slow the intestinal mucosal barrier destruction, and promote the damage repair of cell mucosal barrier.


2017 ◽  
Vol 152 (5) ◽  
pp. S853-S854
Author(s):  
Tadayuki Oshima ◽  
Liping Wu ◽  
Masato Taki ◽  
Toshihiko Tomita ◽  
Yoshio Ohda ◽  
...  

2019 ◽  
Vol 20 (22) ◽  
pp. 5751 ◽  
Author(s):  
Jia Wang ◽  
Cuili Zhang ◽  
Chunmei Guo ◽  
Xinli Li

Ulcerative colitis (UC) has been identified as one of the inflammatory diseases. Intestinal mucosal barrier function and microflora play major roles in UC. Modified-chitosan products have been consumed as effective and safe drugs to treat UC. The present work aimed to investigate the effect of chitosan (CS) on intestinal microflora and intestinal barrier function in dextran sulfate sodium (DSS)-induced UC mice and to explore the underlying mechanisms. KM (Kunming) mice received water/CS (250, 150 mg/kg) for 5 days, and then received 3% DSS for 5 days to induce UC. Subsequently, CS (250, 150 mg/kg) was administered daily for 5 days. Clinical signs, body weight, colon length, and histological changes were recorded. Alterations of intestinal microflora were analyzed by PCR-DGGE, expressions of TNF-α and tight junction proteins were detected by Western blotting. CS showed a significant effect against UC by the increased body weight and colon length, decreased DAI (disease activity index) and histological injury scores, and alleviated histopathological changes. CS reduced the expression of TNF-α, promoted the expressions of tight junction proteins such as claudin-1, occludin, and ZO-1 to maintain the intestinal mucosal barrier function for attenuating UC in mice. Furthermore, Parabacteroides, Blautia, Lactobacillus, and Prevotella were dominant organisms in the intestinal tract. Blautia and Lactobacillus decreased with DSS treatment, but increased obviously with CS treatment. This is the first time that the effect of original CS against UC in mice has been reported and it is through promoting dominant intestinal microflora such as Blautia, mitigating intestinal microflora dysbiosis, and regulating the expressions of TNF-α, claudin-1, occludin, and ZO-1. CS can be developed as an effective food and health care product for the prevention and treatment of UC.


Author(s):  
Siwen Tang ◽  
Wentao Guo ◽  
Liumin Kang ◽  
Jinghua Liang

AbstractTight junction proteins play crucial roles in maintaining the integrity of intestinal mucosal barrier. MiRNA-182-5p is capable of targeting claudin-2 which is one of the vital tight junction proteins and the effect and mechanism of miRNA-182-5p was explored here in the DSS-induced colitis model. The pathological conditions were evaluated via hematoxylin and eosin staining. The gene expression level was assessed via PCR. Quantitative immunohistochemistry analysis was performed for the measurement of claudin-2. microRNA.org online tool was used for target gene prediction. Luciferase reporter assay and RNA pull-down assay were performed to detect the target of miRNA-182-5p. The inflammatory and oxidative stress level were measured using corresponding kits. MiRNA-182-5p was highly expressed in colitis model and miRNA-182-5p inhibitor exerted protective effects on colitis induced by DSS in mice. The protective effects includded improvement of pathological changes, increases in anti-inflammation and anti-oxidative genes, and up-regulation of TGF-β1. Claudin-2 mRNA was predicted as the target of miRNA-182-5p, which was validated via luciferase reporter assay and RNA pull-down assay. Claudin-2 overexpression was found in miRNA-182-5p inhibitor group. Consistent with the role of miRNA-182-5p, claudin-2 overexpression also exerted protective effects on DSS-induced colitis in mice. Inhibition of miRNA-182-5p exerted protective effects on colitis via targeting and upregulating claudin-2. The findings in study provide a new therapeutic strategy for colitis treatment and lay the foundation for future study.


2005 ◽  
Vol 43 (05) ◽  
Author(s):  
Cs Páska ◽  
E Orbán ◽  
A Kiss ◽  
Zs Schaff ◽  
A Szijjártó ◽  
...  

2017 ◽  
Vol 95 (3) ◽  
pp. 1313 ◽  
Author(s):  
L. Zhang ◽  
L. F. Schütz ◽  
C. L. Robinson ◽  
M. L. Totty ◽  
L. J. Spicer

Sign in / Sign up

Export Citation Format

Share Document