scholarly journals Protective effect of Lactobacillus fermentum CQPC04 on dextran sulfate sodium–induced colitis in mice is associated with modulation of the nuclear factor-κB signaling pathway

2019 ◽  
Vol 102 (11) ◽  
pp. 9570-9585 ◽  
Author(s):  
Xianrong Zhou ◽  
Huazhi Liu ◽  
Jing Zhang ◽  
Jianfei Mu ◽  
Zsolt Zalan ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathway ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Nuclear Factor Κb ◽  
Lactobacillus Fermentum ◽  
Nuclear Factor

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 Effect of Iridoid Glycosides of the Leaves of Syringa oblata Lindl. on Dextran Sulfate Sodium-Induced Ulcerative Colitis by Inhibition of the TLR2/4/MyD88/NF-κB Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Yifang Zhang ◽  
Dandan Han ◽  
Shen Yu ◽  
Chiying An ◽  
Xin Liu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Proinflammatory Cytokines ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Iridoid Glycosides ◽  
Mrna Levels ◽  
Dependent Manner

Iridoid glycoside (IG) is the major active fraction extracted from the leaves of Syringa oblata Lindl. In view of its antimicrobial and antidiarrheal potential, it could be beneficial for the treatment of ulcerative colitis (UC). In the present study, IG (20, 40, and 80 mg/kg) was administered orally for 14 days to dextran sulfate sodium- (DSS-) induced colitis rats. The anti-inflammatory effects of IG on DSS-induced UC were evaluated by comparing observations in DSS-induced colitis and drug-treated groups using disease activity index (DAI), macroscopic score, histological analysis, and apoptosis assay. To elucidate the antioxidant mechanisms of IG on NOX-dependent ROS production, the activities of 8-OHdG, NOX1, and NOX2 in DSS-induced colitis were determined. The levels of proinflammatory cytokines such as IL-2, IL-4, IL-5, IL-12p40, and IL-13 were detected. The inflammation-associated protein and mRNA expressions of TLR-2, TLR-4, MyD88, and NF-κBp65 were assessed by immunohistochemistry and real-time quantitative PCR, respectively. The results suggested that IG treatment significantly reduced DAI, macroscopic score, and histological damage compared to untreated animals (p<0.01), whereas administration of IG remarkably attenuated the upregulation of 8-OHdG, NOX1, and NOX2 and the expression of proinflammatory cytokines such as IL-2, IL-4, IL-5, IL-12p40, and IL-13 in DSS-treated rats in a concentration-dependent manner. In addition, IG treatment could dose dependently suppress the protein and mRNA levels of TLR-2, TLR-4, MyD88, and NF-κBp65. The dose of IG that produced the most significant protective effect was 80 mg/kg. The above results demonstrate that IG exerts its inhibitory effect on cell apoptosis, oxidative stress, and proinflammatory cytokines in DSS-induced colitis through modulation of the TLR2/4/MyD88/NF-κB signaling pathway.

Parthenolide, an inhibitor of the nuclear factor-κB pathway, ameliorates dextran sulfate sodium-induced colitis in mice

2012 ◽  
Vol 12 (1) ◽  
pp. 169-174 ◽  
Author(s):  
Zhi Jing Zhao ◽  
Jun Ying Xiang ◽  
Liu Liu ◽  
Xiao Li Huang ◽  
Hua Tian Gan
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

Tetrandrine ameliorates dextran-sulfate-sodium-induced colitis in mice through inhibition of nuclear factor -κB activation

2008 ◽  
Vol 24 (1) ◽  
pp. 5-12 ◽  
Author(s):  
Dei Kui Zhang ◽  
Li Na Cheng ◽  
Xiao Li Huang ◽  
Wei Shi ◽  
Jun Ying Xiang ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

Amelioration of murine dextran sulfate sodium-induced colitis by nuclear factor-κb decoy oligonucleotides

2009 ◽  
Vol 197 (6) ◽  
pp. 797-805 ◽  
Author(s):  
Jun Ying Xiang ◽  
Li Guo Wu ◽  
Xiao Li Huang ◽  
Meng Zhang ◽  
Lan Pen ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

scholarly journals Shikonin Prevents Early Phase Inflammation Associated with Azoxymethane/Dextran Sulfate Sodium-Induced Colon Cancer and Induces Apoptosis in Human Colon Cancer Cells

Planta Medica ◽  
2018 ◽  
Vol 84 (09/10) ◽  
pp. 674-683 ◽  
Author(s):  
Isabel Andújar ◽  
Alberto Martí-Rodrigo ◽  
Rosa Giner ◽  
José Ríos ◽  
María Recio
Keyword(s):  
Nitric Oxide ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Nuclear Factor Κb ◽  
Cancer Development ◽  
Myeloperoxidase Activity ◽  
Nuclear Factor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

AbstractShikonin is the main active principle in the root of Lithospermum erythrorhizon, widely used in traditional Chinese medicine for its anti-inflammatory and wound healing properties. Recent research highlights shikoninʼs antitumor properties and capacity to prevent acute ulcerative colitis. The aim of the present study was to evaluate the ability of shikonin to prevent, in vivo, the early phases of colorectal cancer development, with special focus on its cytotoxic mechanism in vitro. We employed the azoxymethane/dextran sulfate sodium model of colitis in Balb/C mice. Body weight and drinking were monitored throughout the experiment, and length of colon and lesions of the colon were recorded on termination of the experiment in all of the experimental groups. Colons underwent histological evaluation and biochemical analyses [myeloperoxidase activity assay, measurement of interleukin-6, evaluation of proinflammatory enzymes (cyclooxygenase-2 and inducible nitric oxide synthase), and nuclear factor-κB activation by Western blot]. Caco-2 cells were used to evaluate, in vitro, the effect of shikonin on proliferation, cytotoxicity, cell cycle, and apoptosis. Our results reveal that shikonin significantly protected the intestinal tissue of our animals by preventing the shortening of the colorectum and ulcer formation in a dose-dependent manner. Shikonin attenuated the expression of cyclooxygenase-2 and inducible nitric oxide synthase, and myeloperoxidase activity, and inhibited the production of interleukin-6 and activation of nuclear factor-κB. It induced Bcl-2 and inhibited caspase 3. In conclusion, shikonin acts as a chemopreventive agent in the azoxymethane/dextran sulfate sodium model through inhibition of the proinflammatory milieu generated during the disease, an important risk factor in cancer development.

Sign in / Sign up

Export Citation Format

Share Document