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DOI 10.4103/2277-9175.140666

Медицинская библиотека · Advanced biomedical research · 2014

Inflammatory cells' role in acetic acid-induced colitis.

Sanei Mohammad H, Hadizadeh Fatemeh, Adibi Peyman, Alavi Sayyed Ali

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Аннотация

BACKGROUND

FREE RADICALS ARE THE KNOWN MECHANISMS RESPONSIBLE FOR INDUCING COLITIS WITH TWO ORIGINS: Inflammatory cells and tissues. Only the inflammatory cells can be controlled by corticosteroids. Our aim was to assess the importance of neutrophils as one of the inflammatory cells in inducing colitis and to evaluate the efficacy of corticosteroids in the treatment of inflammatory bowel disease (IBD).

MATERIALS AND

METHODS

Thirty-six mice were divided into six groups of six mice each. Colitis was induced in three groups by exposing them to acetic acid through enema (group 1), ex vivo (group 3), and enema after immune suppression (group 5). Each group had one control group that was exposed to water injection instead of acetic acid. Tissue samples were evaluated and compared based on macroscopic damages and biochemical and pathological results.

RESULTS

Considering neutrophilic infiltration, there were significant differences between groups 1, 3, 5, and the control of group 1. Groups 3, 5, and their controls, and group 1 and the control of group 3 had significant differences in terms of goblet depletion. Based on tissue originated H2O2, we found significant differences between group 1 and its control and group 3, and also between groups 5 and the control of group 3. All the three groups were significantly different from their controls based on Ferric Reducing Ability of Plasma (FRAP) and such differences were also seen between group 1 with two other groups.

CONCLUSION

Neutrophils may not be the only cause of oxidation process in colitis, and also makes the effectiveness of corticosteroids in the treatment of this disease doubtful.

Для цитирования: Sanei Mohammad H, Hadizadeh Fatemeh, Adibi Peyman, Alavi Sayyed Ali. Inflammatory cells' role in acetic acid-induced colitis.. Advanced biomedical research. 2014. DOI: 10.4103/2277-9175.140666.
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