Conventional drug therapy for inflammatory bowel disease

Bryant, Robert V.; Brain, Oliver; Travis, Simon

doi:10.3109/00365521.2014.968864

Cited by 63 publications

(61 citation statements)

References 216 publications

(310 reference statements)

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“…2 During IBDs, the integrity of the intestinal layer is damaged and ingested materials and pathogens can cause inflammation by activating the epithelial cells, polymorphonuclear neutrophils, and macrophages to produce inflammatory cytokines and other mediators that further contribute to oxidative stress and perpetuate the inflammatory response in the gut. 8,9 Thus, there is great interest to find new therapeutic strategies for the treatment of IBDs. 4,5 In particular, IBDs are associated with a disequilibrium between ROS and the antioxidant response, giving rise to oxidative stress 6 which is presently considered as potentially critical in the pathogenesis, progression, and severity of IBDs.…”

Section: Introductionmentioning

confidence: 99%

Plumericin prevents intestinal inflammation and oxidative stress in vitro and in vivo

et al. 2019

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Inflammatory bowel diseases (IBDs) are characterized by an inflammatory and oxidative stress condition in the intestinal tissue. In this study, we evaluated the effect of plumericin, one of the main bioactive components of Himatanthus sucuuba (Woodson) bark, on intestinal inflammation and oxidative stress, both in vitro and in vivo. The effect of plumericin (0.5‐2 µM) in vitro was evaluated in rat intestinal epithelial cells (IEC‐6) treated with lipopolysaccharides from E. coli (10 μg/mL) plus interferon‐γ (10 U/mL). Moreover, a 2,4,6‐dinitrobenzene sulfonic acid (DNBS)‐induced colitis model was used to evaluate the anti‐inflammatory and antioxidant activity of plumericin (3 mg/kg) in vivo. The results showed that plumericin significantly reduces intestinal inflammatory factors such as tumor necrosis factor‐α, cyclooxygenase‐2 and inducible nitric oxide synthase expression, and nitrotyrosine formation. Plumericin also inhibited nuclear factor‐κB translocation, reactive oxygen species (ROS) release, and inflammasome activation. Moreover, plumericin activated the nuclear factor erythroid‐derived 2 pathway in IEC‐6. Using the DNBS‐induced colitis model, a significant reduction in the weight loss and in the development of the macroscopic and histologic signs of colon injury, together with a reduced inflammatory and oxidative stress state, were observed in plumericin‐treated mice. These results indicate that plumericin exerts a strong anti‐inflammatory and antioxidant activity. Thus, it might be a candidate for the development of a new pharmacologic approach for IBDs treatment.

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Section: Introductionmentioning

confidence: 99%

Plumericin prevents intestinal inflammation and oxidative stress in vitro and in vivo

et al. 2019

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“…1,2 While the clinical features of Crohn's disease include pain, diarrhea, narrowing of the intestine's lumen leading to structural and bowel obstruction, abscess formation, and fistulization of the skin and internal organs; the clinical features of UC include severe diarrhea, blood loss, and progressive loss of the peristaltic function. However, due to the high risks of adverse effects such as sleep and mood disturbances, dyspepsia, or glucose intolerance, cortico-steroids are not suitable as long term therapies, 5 and new strategies for adjunct therapies are needed. 4 UC can be treated with a number of medications including 5-ASA drugs such as sulfasalazine and mesalazine.…”

Section: Introductionmentioning

confidence: 99%

Oat β-glucan ameliorates dextran sulfate sodium (DSS)-induced ulcerative colitis in mice

et al. 2015

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Ulcerative colitis is a major inflammatory bowel disease (IBD), characterized by inflammation within the gastrointestinal tract through chronic or relapsing immune system activation. The aim of this study is to investigate the potential protective effect of oat β-glucan (βG) against colitis induced by DSS in mice. Eighty mice were randomly divided into the control group (no DSS, no βG), DSS group (DSS only), DSS + L-βG group (DSS plus 500 mg per kg βG), and DSS + H-βG group (DSS plus 1000 mg per kg βG). Compared with the DSS group, administration of βG significantly reduced clinical symptoms with less weight loss, diarrhea and shortening of the colon, the severity of colitis was significantly inhibited as evidenced by the reduced disease activity index (DAI) and degree of histological damage in colon. Moreover, treatment with βG not only decreased myeloperoxidase activity (MPO), and nitric oxide (NO) and malondialdehyde (MDA) levels, but also inhibited mRNA and protein expression of pro-inflammatory factors such as TNF-α, IL-1β, IL-6 and iNOS. This suggests that oat βG in diet might exhibit an anti-inflammatory function against colitis through inhibition of expression of pro-inflammatory factors.

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“…Intestinal mucosal inflammation can lead to sustained and irreversible damage to the digestive tract and produce serious clinical consequences (6). A variety of inflammatory mediators such as interleukin (IL)-4, IL-1, tumor necrosis factor and transforming growth factor (TGF)-β, as well as several signal pathways such as the nuclear factor-κB signaling pathway, participate in the damage of the digestive tract (7–9).…”

Section: Introductionmentioning

confidence: 99%

Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy

Zhao

Wei

et al. 2016

Experimental and Therapeutic Medicine

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The aim of this study was to investigate the expression of decorin (DCN) in the intestinal tissues of mice with inflammatory bowel disease (IBD) and its correlation with autophagy. The IBD mouse model was created by intrarectal injection of trinitrobenzene sulfonic acid. The pathology of colon tissues of the mice was examined using hematoxylin and eosin staining. Expression of DCN and the proteins associated with autophagy was detected using immunohistochemistry. Normal human colon mucosal epithelial cells (NCM460 cells) were transfected with DCN expression plasmid and the expression of DCN and autophagy-associated proteins was detected by western blot analysis. Cell apoptosis was studied using an Annexin V apoptosis detection assay and intracellular autophagosomes were observed using electron microscopy. The IBD mouse model was successfully established. Thickening, edema and inflammatory cell infiltration of the intestinal wall were observed in the IBD mice. The expression of DCN as well as the autophagy-associated proteins beclin 1 and LC3B, was increased in the intestinal tissues of the IBD mice. Furthermore, in the NCM460 cells transfected with DCN, the expression of beclin 1 and LC3B was upregulated, while p62 expression was downregulated. Intracellular autophagosomes were increased and apoptosis was decreased in the cells with DCN overexpression. Inhibition of autophagy reversed the effects of DCN on apoptosis. Therefore, DCN is able to induce autophagy and protect intestinal cells during the occurrence and development of IBD.

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Conventional drug therapy for inflammatory bowel disease

Cited by 63 publications

References 216 publications

Plumericin prevents intestinal inflammation and oxidative stress in vitro and in vivo

Plumericin prevents intestinal inflammation and oxidative stress in vitro and in vivo

Oat β-glucan ameliorates dextran sulfate sodium (DSS)-induced ulcerative colitis in mice

Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy

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