Oral administration of the flavonoid myricitrin prevents dextran sulfate sodium-induced experimental colitis in mice through modulation of PI3K/Akt signaling pathway

2013 ◽  
Vol 57 (11) ◽  
pp. 1938-1949 ◽  
Author(s):  
Raquel Cristina Schwanke ◽  
Rodrigo Marcon ◽  
Flavia Carla Meotti ◽  
Allisson Freire Bento ◽  
Rafael Cypriano Dutra ◽  
...  
Keyword(s):  
Oral Administration ◽  
Signaling Pathway ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Experimental Colitis ◽  
Akt Signaling ◽  
Akt Signaling Pathway

scholarly journals Is dextran sulfate sodium a good inducer of acute experimental enteritis?

2019 ◽  
Vol 33 ◽  
pp. 205873841984336
Author(s):  
Wei Chen ◽  
Jing Zhang ◽  
Chen Li ◽  
Quan Pan ◽  
Jingtong Wu ◽  
...  
Keyword(s):  
Oral Administration ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Experimental Colitis ◽  
The Body ◽  
Control Group ◽  
Average Weight ◽  
Inflammatory Infiltration ◽  
Intestine Length ◽  
Hematoxylin And Eosin

Animal models play critical roles in exploring the pathogenesis of human diseases and designing novel therapeutic schemes. Acute experimental colitis (AEC) models have been reported to be established in mice principally by oral administration of dextran sulfate sodium (DSS). However, little knowledge is known about whether DSS can be used to induce the acute experimental enteritis (AEE). In this study, different concentrations of DSS (0%, 2%, 3%, and 5%) were used to induce AEC and AEE models in two cohorts. After the establishment of these two models, the symptoms of the mice induced by DSS were noted, the length and average weight of each colon and small intestine were measured, and hematoxylin and eosin (HE) staining was conducted for assessing the inflammatory infiltration in these models. Generally, the comparison of the inflammatory scoring between AEC and AEE models was analyzed. As a consequence, we found that, the mice with 2%–5% DSS administration in a week could develop into AEC models in two cohorts and AEE models in one cohort, followed by the signs of diarrhea, gross rectal bleeding, weight loss of the body, and shortened colon and intestine length, as compared with the control group. HE staining showed that the inflammatory scoring was dramatically increased by 3%–5% DSS in AEC models in two cohorts but slightly elevated in AEE models in one cohort. Meanwhile, as compared with the severe AEC models, the extent of inflammatory infiltration induced by 3%–5% DSS in AEE models was much milder. In conclusion, oral administration of 3%–5% DSS is a good inducer of AEC models, but not AEE models.

Hepatocyte growth factor promotes colonic epithelial regeneration via Akt signaling

2007 ◽  
Vol 293 (1) ◽  
pp. G230-G239 ◽  
Author(s):  
Masami Kanayama ◽  
Terumi Takahara ◽  
Yutaka Yata ◽  
Feng Xue ◽  
Eiji Shinno ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Akt Signaling ◽  
Colonic Epithelial Cells ◽  
Hepatocyte Growth

Hepatocyte growth factor (HGF) can promote the regeneration of injured organs, including HGF gene therapy by electroporation (EP) for liver injury. In this study, we investigated the effect of HGF on dextran sulfate sodium-induced colitis and tried to clarify the regenerative mechanisms of colonic epithelial cells and the signaling pathway involved. Colitis was induced by dextran sulfate sodium in mice, together with HGF gene transfer by EP. On day 10, the colitis was evaluated histologically and by Western blot analysis. The colonic epithelial cell line MCE301 was exposed to HGF protein, and its proliferation and activated signaling pathway were analyzed. In vivo, the histological score improved and the number of Ki-67-positive epithelial cells increased in the HGF-treated mice compared with the controls. Western blot analysis showed enhanced expression of phospho-Akt in the HGF-treated mice compared with the controls. In vitro, HGF stimulated the proliferation of MCE301 cells. There was enhanced phospho-Akt expression for more than 48 h after HGF stimulation, although phospho-ERK1/2 was enhanced for only 10 min. LY-294002 or Akt small interfering RNA suppressed cell proliferation induced by HGF. Thus HGF induces the proliferation of colonic epithelial cells via the phosphatidylinositol 3-kinase/Akt signaling pathway. HGF gene therapy can attenuate acute colitis via epithelial cell proliferation through the PI3K/Akt pathway. These data suggested that HGF gene therapy by EP may be effective for the regeneration and repair of injured epithelial cells in inflammatory bowel disease.

scholarly journals Beauvericin Ameliorates Experimental Colitis by Inhibiting Activated T Cells via Downregulation of the PI3K/Akt Signaling Pathway

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e83013 ◽  
Author(s):  
Xue-Feng Wu ◽  
Rui Xu ◽  
Zi-Jun Ouyang ◽  
Cheng Qian ◽  
Yan Shen ◽  
...  
Keyword(s):  
T Cells ◽  
Signaling Pathway ◽  
Experimental Colitis ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Activated T Cells

scholarly journals Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Zeng-Ping Kang ◽  
Meng-Xue Wang ◽  
Tian-Tian Wu ◽  
Duan-Yong Liu ◽  
Hai-Yan Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Signaling Pathway ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Macrophage Polarization ◽  
Experimental Colitis ◽  
The Body ◽  
M2 Macrophage ◽  
Therapeutic Effects ◽  
M2 Macrophage Polarization

Curcumin has shown good efficacy in mice with experimental colitis and in patients with ulcerative colitis, but the mechanism of action through the regulation of M1/M2 macrophage polarization has not been elaborated. The ulcerative colitis was modeled by dextran sulfate sodium; colitis mice were orally administrated with curcumin (10 mg/kg/day) or 5-ASA (300 mg/kg/day) for 14 consecutive days. After curcumin treatment, the body weight, colon weight and length, colonic weight index, and histopathological damage in colitis mice were effectively improved. The concentrations of proinflammatory cytokines IL-1β, IL-6, and CCL-2 in the colonic tissues of colitis mice decreased significantly, while anti-inflammatory cytokines IL-33 and IL-10 increased significantly. Importantly, macrophage activation was suppressed and M1/M2 macrophage polarization was regulated in colitis mice, and the percentage of CD11b+F4/80+ and CD11b+F4/80+TIM-1+ and CD11b+F4/80+iNOS+ decreased significantly and CD11b+F4/80+CD206+ and CD11b+F4/80+CD163+ increased significantly. Additionally, curcumin significantly downregulated CD11b+F4/80+TLR4+ macrophages and the protein levels of TLR2, TLR4, MyD88, NF-κBp65, p38MAPK, and AP-1 in colitis mice. Our study suggested that curcumin exerted therapeutic effects in colitis mice by regulating the balance of M1/M2 macrophage polarization and TLRs signaling pathway.

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