Antioxidant Effects of Dracocephalum kotschyi Extract in the Experimental Colitis Model Induced by Acetic Acid

AbstractDue to the ethnopharmacological use of Campsiandra laurifolia (Fabaceae), popularly known as Acapurana, to treat wounds and ulcers, associated with the lack of alternative treatments for intestinal inflammations such as ulcerative colitis (UC), the present work sought to characterize its phytochemical and antioxidant activities, and to evaluate remedial action in experimental colitis with acetic acid. Phytochemical analyzes were performed through qualitative and quantitative colorimetric tests of the main secondary metabolites. In the colitis model, 24 male Wistar rats aged ± 60 days old were used, divided into 4 groups: Control (CO) control + aqueous extract of C. laurifolia 50 mg/kg (CO + A50); Colitis (CL); and Colitis + aqueous extract of C. laurifolia 50 mg/kg (CL + A50). Measurement of sphincter anal pressure and histological tests of the large intestine, lipoperoxidation (LPO), enzyme activity of superoxide dismutase (SOD), and levels of glutathione (GSH) were performed. For statistical analysis, the oxidative stress (OS) results were expressed as means ± standard error, adopting a significance level of p < 0.05. The screening indicated the presence of flavonoids, saponins and tannins in the extract, with high levels of phenolic compounds and tannins, and was related to high antioxidant capacity. In the histological analysis, the CL group presented loss of the crypts, edema and inflammatory infiltrate. The use of C. laurifolia extract restructured the crypts, decreased edema and increased sphincter anal pressure, with a decrease in LPO, SOD, and an increase in GSH. It is suggested that the use of C. laurifolia extract reduces OS due to its antioxidant power conferred by the phenolic compounds present in the extract.

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Cinnamaldehyde targets TLR-4 and inflammatory mediators in acetic-acid induced ulcerative colitis model

Biologia ◽

10.1007/s11756-021-00725-w ◽

2021 ◽

Author(s):

Saeideh Momtaz ◽

Maryam Navabakhsh ◽

Negin Bakouee ◽

Mustafa Dehnamaki ◽

Mahban Rahimifard ◽

...

Keyword(s):

Ulcerative Colitis ◽

Acetic Acid ◽

Inflammatory Mediators ◽

Colitis Model

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Gut Microbiota-Derived Propionate Regulates the Expression of Reg3 Mucosal Lectins and Ameliorates Experimental Colitis in Mice

Journal of Crohn s and Colitis ◽

10.1093/ecco-jcc/jjaa065 ◽

2020 ◽

Vol 14 (10) ◽

pp. 1462-1472 ◽

Cited By ~ 2

Author(s):

Danica Bajic ◽

Adrian Niemann ◽

Anna-Katharina Hillmer ◽

Raquel Mejias-Luque ◽

Sena Bluemel ◽

...

Keyword(s):

Protective Factor ◽

Experimental Colitis ◽

Short Chain Fatty Acids ◽

Stem Cell Marker ◽

Knock Out ◽

Interleukin 22 ◽

Epithelial Regeneration ◽

Dss Colitis ◽

Colitis Model

Abstract Background and Aims Regenerating islet-derived protein type 3 [Reg3] lectins are antimicrobial peptides at mucosal surfaces of the gut, whose expression is regulated by pathogenic gut microbes via interleukin-22- or Toll-like receptor signalling. In addition to antimicrobial effects, tissue protection is hypothesized, but has been poorly investigated in the gut. Methods We applied antibiotic-induced microbiota perturbations, gnotobiotic approaches and a dextran-sodium sulfate [DSS] colitis model to assess microbial Reg3 regulation in the intestines and its role in colitis. We also used an intestinal organoid model to investigate this axis in vitro. Results First, we studied whether gut commensals are involved in Reg3 expression in mice, and found that antibiotic-mediated reduction of Clostridia downregulated intestinal Reg3B. A loss in Clostridia was accompanied by a significant reduction of short-chain fatty acids [SCFAs], and knock-out [KO] mice for SCFA receptors GPR43 and GPR109 expressed less intestinal Reg3B/-G. Propionate was found to induce Reg3 in intestinal organoids and in gnotobiotic mice colonized with a defined, SCFA-producing microbiota. Investigating the role of Reg3B as a protective factor in colitis, we found that Reg3B-KO mice display increased inflammation and less crypt proliferation in the DSS colitis model. Propionate decreased colitis and increased proliferation. Treatment of organoids exposed to DSS with Reg3B or propionate reversed the chemical injury with a loss of expression of the stem-cell marker Lgr5 and Olfm4. Conclusions Our results suggest that Clostridia can regulate Reg3-associated epithelial homeostasis through propionate signalling. We also provide evidence that the Reg3–propionate axis may be an important mediator of gut epithelial regeneration in colitis.

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Protective effect of marine mangrove Rhizophora apiculata on acetic acid induced experimental colitis by regulating anti-oxidant enzymes, inflammatory mediators and nuclear factor-kappa B subunits

International Immunopharmacology ◽

10.1016/j.intimp.2013.11.007 ◽

2014 ◽

Vol 18 (1) ◽

pp. 124-134 ◽

Cited By ~ 18

Author(s):

Vinod Prabhu V. ◽

Guruvayoorappan C.

Keyword(s):

Acetic Acid ◽

Protective Effect ◽

Inflammatory Mediators ◽

Nuclear Factor Kappa B ◽

Experimental Colitis ◽

Nuclear Factor ◽

Nuclear Factor Kappa ◽

Rhizophora Apiculata ◽

Anti Oxidant ◽

B Subunits

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B cell activation in the cecal patches during the development of an experimental colitis model

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2018.01.053 ◽

2018 ◽

Vol 496 (2) ◽

pp. 367-373 ◽

Cited By ~ 2

Author(s):

Taro Watabe ◽

Takashi Nagaishi ◽

Naoya Tsugawa ◽

Yudai Kojima ◽

Nisha Jose ◽

...

Keyword(s):

B Cell ◽

Cell Activation ◽

Experimental Colitis ◽

B Cell Activation ◽

Colitis Model

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High-fat diet promotes experimental colitis by inducing oxidative stress in the colon

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00103.2019 ◽

2019 ◽

Vol 317 (4) ◽

pp. G453-G462 ◽

Cited By ~ 9

Author(s):

Xue Li ◽

Xinzhi Wei ◽

Yue Sun ◽

Jie Du ◽

Xin Li ◽

...

Keyword(s):

Oxidative Stress ◽

High Fat Diet ◽

Experimental Colitis ◽

Mucosal Barrier ◽

Mucosal Inflammation ◽

High Fat ◽

Trinitrobenzenesulfonic Acid ◽

Barrier Permeability ◽

Inflammatory Bowel ◽

Colitis Model

Diets high in animal fats are associated with increased risks of inflammatory bowel disease, but the mechanism remains unclear. In this study, we investigated the effect of high-fat diet (HFD) on the development of experimental colitis in mice. Relative to mice fed low-fat diet (LFD), HFD feeding for 4 wk increased the levels of triglyceride, cholesterol, and free fatty acids in the plasma as well as within the colonic mucosa. In an experimental colitis model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS), mice on 4-wk HFD exhibited more severe colonic inflammation and developed more severe colitis compared with the LFD counterparts. HFD feeding resulted in higher production of mucosal pro-inflammatory cytokines, greater activation of the myosin light chain kinase (MLCK) tight junction regulatory pathway, and greater increases in mucosal barrier permeability in mice following TNBS induction. HFD feeding also induced gp91, an NADPH oxidase subunit, and promoted reactive oxygen species (ROS) production in both colonic epithelial cells and lamina propria cells. In HCT116 cell culture, palmitic acid or palmitic acid and TNF-α combination markedly increased ROS production and induced the MLCK pathway, and these effects were markedly diminished in the presence of a ROS scavenger. Taken together, these data suggest that HFD promotes colitis by aggravating mucosal oxidative stress, which rapidly drives mucosal inflammation and increases intestinal mucosal barrier permeability. NEW & NOTEWORTHY This study demonstrates high-fat diet feeding promotes colitis in a 2,4,6-trinitrobenzenesulfonic acid-induced experimental colitis model in mice. The underlying mechanism is that high-fat diet induces oxidative stress in the colonic mucosa, which increases colonic epithelial barrier permeability and drives colonic mucosal inflammation. These observations provide molecular evidence that diets high in saturated fats are detrimental to patients with inflammatory bowel diseases.

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