Protective effects of polysaccharides from Atractylodes macrocephalae Koidz. against dextran sulfate sodium induced intestinal mucosal injury on mice

2021 ◽  
Author(s):  
Lixia Kai ◽  
Xin Zong ◽  
Qin Jiang ◽  
Zeqing Lu ◽  
Fengqin Wang ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Mucosal Injury ◽  
Protective Effects ◽  
Intestinal Mucosal Injury

scholarly journals EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Xue Bing ◽  
Liu Xuelei ◽  
Dong Wanwei ◽  
Liang Linlang ◽  
Chen Keyan
Keyword(s):  
Ulcerative Colitis ◽  
Flow Cytometry ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Mucosal Injury ◽  
Inflammatory Factors ◽  
Intestinal Mucosal Injury

Objective. To observe the protective effect of epigallocatechin gallate (EGCG) on dextran sulfate sodium- (DSS-) induced ulcerative colitis in rats and to explore the roles of TLR4/MyD88/NF-κB signaling pathway. Methods. Rat models of ulcerative colitis were established by giving DSS. EGCG (50 mg/kg/d) was given to assess disease activity index. HE staining was applied to observe histological changes. ELISA and qPCR detected the expression of inflammatory factors. Flow cytometry was used to measure the percentage of CD4+IFN-γ+ and CD4+IL-4+ in the spleen and colon. TLR4 antagonist E5564 was given in each group. Flow cytometry was utilized to detect CD4+IFN-γ+ and CD4+IL-4+ cells. Immunohistochemistry, qPCR, and western blot assay were applied to measure the expression of TLR4, MyD88, and NF-κB. Results. EGCG improved the intestinal mucosal injury in rats, inhibited production of inflammatory factors, maintained the balance of Th1/Th2, and reduced the expression of TLR4, MyD88, and NF-κB. After TLR4 antagonism, the protective effect of EGCG on intestinal mucosal injury was weakened in rats with ulcerative colitis, and the expressions of inflammatory factors were upregulated. Conclusion. EGCG can inhibit the intestinal inflammatory response by reducing the severity of ulcerative colitis and maintaining the Th1/Th2 balance through the TLR4/MyD88/NF-κB signaling pathway.

scholarly journals Protective effects of glycoglycerolipids extracted from spinach on 5-fluorouracil induced intestinal mucosal injury

2010 ◽  
Vol 57 (3,4) ◽  
pp. 314-320 ◽  
Author(s):  
Asuka Shiota ◽  
Takahiko Hada ◽  
Tomoko Baba ◽  
Minako Sato ◽  
Hisami Yamanaka-Okumura ◽  
...  
Keyword(s):  
Mucosal Injury ◽  
Protective Effects ◽  
Intestinal Mucosal Injury

scholarly journals Protective Effects of L-Theanine on IPEC-J2 Cells Growth Inhibition Induced by Dextran Sulfate Sodium Via p53 Signaling Pathway

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 7002
Author(s):  
Longlin Zhang ◽  
Mengmeng Ma ◽  
Zhengyi Li ◽  
Haihan Zhang ◽  
Xi He ◽  
...  
Keyword(s):  
Amino Acid ◽  
Signaling Pathway ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Nucleotide Metabolism ◽  
Normal Operation ◽  
Protective Effects ◽  
P53 Signaling ◽  
P53 Signaling Pathway

L-theanine is a nonprotein amino acid found in tea leaves and has been widely used as a safe food additive in beverages or foods because of its varied bioactivities. The aim of this study was to reveal the in vitro gastrointestinal protective effects of L-theanine in DSS-induced intestinal porcine enterocyte (IPEC-J2) cell models using molecular and metabolic methods. Results showed that 2.5% dextran sulfate sodium (DSS) treatment inhibited the cell proliferation of IPEC-J2 and blocked the normal operation of the cell cycle, while L-theanine pretreatment significantly preserved these trends to exert protective effects. L-theanine pre-treatment also up-regulated the EGF, CDC2, FGF2, Rb genes and down-regulated p53, p21 proliferation-related mRNA expression in DSS-treated cells, in accompany with p53 signaling pathway inhibition. Meanwhile, metabolomics analysis revealed that L-theanine and DSS treated IPEC-J2 cells have different metabolomic profiles, with significant changes in the key metabolites involved in pyrimidine metabolism and amino acid metabolism, which play an important role in nucleotide metabolism. In summary, L-theanine has a beneficial protection in DSS-induced IPEC-J2 cells via promoting proliferation and regulating metabolism disorders.

Protective effects of betulinic acid on intestinal mucosal injury induced by cyclophosphamide in mice

2019 ◽  
Vol 71 (5) ◽  
pp. 929-939 ◽  
Author(s):  
Xihong Wang ◽  
Zhihang Yuan ◽  
Lijuan Zhu ◽  
Xianglian Yi ◽  
Zhaoping Ou ◽  
...  
Keyword(s):  
Betulinic Acid ◽  
Mucosal Injury ◽  
Protective Effects ◽  
Intestinal Mucosal Injury

scholarly journals Probiotic Mixture Protects Dextran Sulfate Sodium-Induced Colitis by Altering Tight Junction Protein Expressions and Increasing Tregs

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Yingdi Zhang ◽  
Xiaojing Zhao ◽  
Yunjuan Zhu ◽  
Jingjing Ma ◽  
Haiqin Ma ◽  
...  
Keyword(s):  
Tight Junction ◽  
Peripheral Blood ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Protective Effects ◽  
Junction Protein

Bifico is a probiotic mixture containing Bifidobacterium, Lactobacillus acidophilus, and Enterococcus. Studies support that Bifico has a protective effect in experimental colitis (IL-10-deficient and TNBS) models and in patients with inflammatory bowel disease (IBD). However, the mechanism underlying the protective effects of this mixture of probiotic bacteria remains incompletely clear. Here, we investigated the effect of Bifico on intestinal inflammation. In an in vivo experiment, dextran sulfate sodium was used to induce colitis. Bifico treatment significantly attenuated the severity of colitis in this model. Bifico increased the expression of tight junction proteins (TJs). In addition, Bifico increased the number of Tregs, but reduced the number of total CD4+ T cells in the peripheral blood. Furthermore, the expression of colonic CD4 protein was decreased while the level of forkhead box P3 (Foxp3) was upregulated. These results suggested that Bifico exerts beneficial effects on experimental colitis by increasing the expressions of TJs, upregulating the number of Tregs, and reducing the total CD4+ T cell number in both colon and peripheral blood. The intestinal damage in the pretreated + treated-Bifico-colitis group was more severe than that in only the pretreated-Bifico-colitis group. This suggested that Bifico might aggravate intestinal damage when the mucosal barrier is impaired.

scholarly journals Suppression of Dextran Sulfate Sodium-Induced Colitis in Mice by Radon Inhalation

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Yuichi Nishiyama ◽  
Takahiro Kataoka ◽  
Keiko Yamato ◽  
Takehito Taguchi ◽  
Kiyonori Yamaoka
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Disease Activity Index ◽  
Myeloperoxidase Activity ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Activated Neutrophils ◽  
Radon Inhalation ◽  
Activity Index Score

The enhanced release of reactive oxygen species from activated neutrophils plays important role in the pathogenesis of inflammatory bowel disease. We previously reported that radon inhalation activates antioxidative functions in various organs of mice. In this study, we examined the protective effects of radon inhalation on dextran sulfate sodium- (DSS) induced colitis in mice which were subjected to DSS for 7 days. Mice were continuously treated with air only (sham) or radon at a concentration of 2000 Bq/m3from a day before DSS administration to the end of colitis induction. In the results, radon inhalation suppressed the elevation of the disease activity index score and histological damage score induced by DSS. Based on the changes in tumor necrosis factor-alpha in plasma and myeloperoxidase activity in the colon, it was shown that radon inhalation suppressed DSS-induced colonic inflammation. Moreover, radon inhalation suppressed lipid peroxidation of the colon induced by DSS. The antioxidant level (superoxide dismutase and total glutathione) in the colon after DSS administration was significantly higher in mice treated with radon than with the sham. These results suggested that radon inhalation suppressed DSS-induced colitis through the enhancement of antioxidative functions in the colon.

scholarly journals The Potential of Vitamin D3 to Repaired Mucosal Injury in Dextran Sulfate Sodium Induced Acute Colitis in Mice

2021 ◽  
Vol 9 (B) ◽  
pp. 931-936
Author(s):  
Satrio Wibowo ◽  
Krisni Subandiyah ◽  
Kusworini Handono ◽  
Sri Poeranto
Keyword(s):  
Stem Cell ◽  
Vitamin D3 ◽  
Cell Activation ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Disease Activity Index ◽  
Mucosal Injury ◽  
Potential Effect ◽  
Mucosal Repair

BACKGROUND: Inflammatory Bowel Disease (IBD) has become an emerging disease worldwide. The treatment of IBD involves two basic principles: Inflammation control and mucosal repair. AIM: This study evaluates the potential effect of Vitamin D3 in mucosal repair through colon stem cell activation and proliferation. METHODS: Dextran sulfate sodium (DSS; 5%) was used to induce colitis in mice. Vitamin D3 at various dosages was then administered as a treatment. The mice were divided into five groups: Control (C-); DSS only (C+); and DSS (5%) plus Vitamin D3 at 0.2 μg (VD1), 0.4 μg (VD2), or 0.6 μg (VD3) per 25 g body weight as the treatment groups. Immunofluorescence analyses of Lgr5+ expression indicated stem cell activation, and Ki67 expression indicated stem cell proliferation. The disease activity index (DAI), colon length, and histopathological index scores were determined after treatment to assess the inflammation and severity of colitis. RESULTS: Immunofluorescence analyses showed a gradually increasing expression of Lgr5+ also Ki67 in proportion with high doses group of Vitamin D3 (p < 0.05). The colon length, DAI scores, and histopathological index scores improved in all groups after Vitamin D3 treatment (p = 0.05; p = 0.026; and p = 0.029, respectively). CONCLUSION: Vitamin D3 has a potential beneficial effect on amplifying intestinal stem cells regulated by Wnt/B-catenin signaling. It is also reduced the inflammatory process proved by the evaluation severity of colitis. It might play an essential role in mucosal repair in IBD.

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