Inflammatory bowel disease in rats: Bacterial and chemical interaction

Hussein, Inaya Abdallah Hajj; Tohme, Rania A.; Barada, Kassem; Mostafa, Mostafa Hassan; Freund, Jean–Noël; Jurjus, Rosalyn A.; Karam, Walid; Jurjus, A

doi:10.3748/wjg.14.4028

Cited by 30 publications

(28 citation statements)

References 38 publications

(68 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our study, MPO activity was significantly increased (p<0.01) by the intrarectal injection of acetic acid and decreased (p<0.05) by administration of Se and vitamin E (Table 3). These results are in accordance with the results of the studies showing MPO activity increase in experimental colitis [7,18,38].…”

Section: Discussionsupporting

confidence: 95%

Protective Effects of Selenium and Vitamin E Combination on Experimental Colitis in Blood Plasma and Colon of Rats

Bıtıren

Karakılçık

Zerin

et al. 2009

Biol Trace Elem Res

View full text Add to dashboard Cite

Ulcerative colitis increases oxidative damage accompanied by production of free oxygen radicals. Selenium (Se) and vitamin E are two natural antioxidants. The present study was undertaken to investigate the possible protective role of Se and vitamin E combination in experimental colitis induced by acetic acid (AA) in rats. This study was carried out on three groups, namely the first (control), the second (experimental colitis group, 2 ml 5% acetic acid), and the third groups (2 ml 5% acetic acid, vitamin E (100 mg/kg body weight (bw)) plus Se (0.2 mg/kg bw)). The activities of catalase (CAT), prolidase (PRS), myeloperoxidase (MPO), total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI), total thiol (T-SH) were determined in plasma and colon samples. Macroscopic and microscopic damages in colon were increased by AA treatment (p < 0.01 and p < 0.01, respectively), whereas they were decreased by selenium and vitamin E treatment (p < 0.05 and p < 0.01, respectively). The activities of CAT and PRS in the plasma and colon were significantly affected (p < 0.05 and p < 0.01) by treatment of AA, Se, and vitamin E. MPO activity in colon was increased (p < 0.01) by AA treatment and decreased (p < 0.05) by Se and vitamin E administration. The values of TOS and OSI in plasma were increased (p < 0.5) by AA. The TAC and T-SH in colon were decreased (p < 0.05) by AA and increased (p < 0.05) by Se and vitamin E. Based upon these results, Se and vitamin E may play an important role in preventive indication of the oxidative damage associated by acetic acid caused inflammation.

show abstract

Section: Discussionsupporting

confidence: 95%

Protective Effects of Selenium and Vitamin E Combination on Experimental Colitis in Blood Plasma and Colon of Rats

Bıtıren

Karakılçık

Zerin

et al. 2009

Biol Trace Elem Res

View full text Add to dashboard Cite

show abstract

“…There was increased MPO activity in the DSS-induced colitis mouse model, implying that leukocytes were recruited. These results were in accordance with the prior studies showing an increase in MPO activity in experimental colitis [29,30]. MPO catalyzes the formation of such potent cytotoxic oxidants as HOCl from H 2 O 2 , chloride ions and N-chloramines in neutrophils [31].…”

Section: Discussionsupporting

confidence: 93%

Polydatin Ameliorates DSS-Induced Colitis in Mice through Inhibition of Nuclear Factor-kappaB Activation

Yao

Wang²,

Liu³

et al. 2010

Planta Med

View full text Add to dashboard Cite

Nuclear factor- κB (NF- κB) plays a pivotal role in the regulation of immune and inflammatory responses. The real-time expression level of NF- κB reflects the development of ulcerative colitis (UC). Polydatin has vast pharmacological activities, including inhibiting the production of inflammatory mediators, inducing the production of antioxidants, regulating immune function, etc. The purpose of this study was to investigate the potential inhibitory effects of polydatin on NF- κB pathway activation in a mouse UC model. The results showed that polydatin treatment downregulated NF- κB p65 activity and expression, blocked the expression of TNF- α, IL-6 and IL-1 β at both mRNA and protein levels, decreased myeloperoxidase (MPO) activity, and alleviated inflammatory damage of colitis in mice with UC (p < 0.05), suggesting that the anti-inflammation effects of polydatin can be attributed, at least partially, to the blocking of the NF- κB pathway.

show abstract

“…Most of the commensal bacteria are symbiotic; however, they could cause pathology after their translocation to the mucosa or under specific conditions. The largest number of bacterial cells is found in the large intestine (10 11 per gram of intestinal content), the main geography of IBD and CRC [19] , [41] .…”

Section: Introductionmentioning

confidence: 99%

Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links

et al. 2016

Self Cite

View full text Add to dashboard Cite

The co-occurrence of the three disease entities, inflammatory bowel disease (IBD), colorectal cancer (CRC), type 2diabetes mellitus (T2DM) along with inflammation and dismicrobism has been frequently reported. Some authors have even suggested that dysbiosis could be the link through a molecular crosstalk of multiple inflammatory loops including TGFβ, NFKB, TNFα and ROS among others.This review focuses on the inflammatory process along with the role of microbiota in the pathophysiology of the three diseases.The etiology of IBD is multifactorial, and like CRC and T2DM, it is associated with a widespread and sustained GI inflammation and dismicrobism, whereby an array of pro-inflammatory mediators and other related biomolecules are up-regulated, both locally and systematically. Such a persistent or an inadequately resolved chronic inflammation may be a causative agent, in the presence other factors, leading to several pathologies such as IBD, CRC and T2DM.TGFβ plays a crucial role in pancreatic β cell malfunctioning as glucotoxicity stimulates its signaling cascade through smad 3, IL-6 and epithelial to mesenchymal transition. Such a cascade could lead to macrophages and other cells recruitment, inflammation, then IBD and CRC.NFkB is also another key regulator in the crosstalk among the pathways leading to the three disease entities. It plays a major role in linking inflammation to cancer development through its ability to up regulate several inflammatory and tumor promoting cytokines like: IL-6, IL-1 α and TNF α, as well as genes like BCL2 and BCLXL. It activates JAK/STAT signaling network via STAT3 transcription factors and promotes epithelial to mesenchymal transition. It also increases the risk for T2DM in obese people. In brief, NFKB is a matchmaker between inflammation, IBD, cancer and diabetes.In addition, TNFα plays a pivotal role in systemic inflammation. It is increased in the mucosa of IBD patients and has a central role in its pathogenesis. It also activates other signaling pathways like NFKB and MAPK leading to CRC. It is also overexpressed in the adipose tissues of obese patients thus linking it to T2DM, chronic inflammation and consequently CRC.On the other hand, increasing evidence suggests that dysbiosis plays a role in initiating, maintaining and determining the severity of IBD. Actually, among its functions, it modulates genotoxic metabolites which are able to induce CRC, a fact proven to be sustained by stool transfer from patients with CRC. Probiotics, however, may actively prevent CRC as well as IBD and results in a significant decrease in fasting glycemia in T2DM patients.In conclusion, IBD, CRC and T2DM are commonly occurring interrelated clinical problems. They share a common basis influenced by an inflammatory process, an imbalance in intestinal microbiota, and a crosstalk between various signaling pathways. Would probiotics interrupt the crosstalk or orient it in the physiological direction?

show abstract

Inflammatory bowel disease in rats: Bacterial and chemical interaction

Cited by 30 publications

References 38 publications

Protective Effects of Selenium and Vitamin E Combination on Experimental Colitis in Blood Plasma and Colon of Rats

Protective Effects of Selenium and Vitamin E Combination on Experimental Colitis in Blood Plasma and Colon of Rats

Polydatin Ameliorates DSS-Induced Colitis in Mice through Inhibition of Nuclear Factor-kappaB Activation

Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links

Contact Info

Product

Resources

About