炎症细胞在乙酸诱导的结肠炎中的作用。

Inflammatory cells' role in acetic acid-induced colitis.

作者信息

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

机构信息

Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Integrated Functional Gastroenterology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran ; East Sage Co, Isfahan Science and Technology Town, Isfahan, Iran.

出版信息

Adv Biomed Res. 2014 Sep 23;3:193. doi: 10.4103/2277-9175.140666. eCollection 2014.

Abstract

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.

摘要

背景

自由基是已知的引发结肠炎的机制,其来源有两个:炎症细胞和组织。只有炎症细胞可被皮质类固醇控制。我们的目的是评估中性粒细胞作为引发结肠炎的炎症细胞之一的重要性,并评估皮质类固醇在治疗炎症性肠病(IBD)中的疗效。

材料与方法

36只小鼠被分为6组,每组6只。通过灌肠(第1组)、体外(第3组)和免疫抑制后灌肠(第5组)使三组小鼠诱发结肠炎。每组有一个对照组,对照组接受水注射而非醋酸。根据宏观损伤以及生化和病理结果对组织样本进行评估和比较。

结果

考虑到中性粒细胞浸润,第1、3、5组与第1组的对照组之间存在显著差异。第3、5组及其对照组,以及第1组和第3组的对照组在杯状细胞减少方面存在显著差异。基于组织源性过氧化氢,我们发现第1组与其对照组以及第3组之间存在显著差异,第5组与第3组的对照组之间也存在显著差异。基于血浆铁还原能力(FRAP),所有三组与各自的对照组均存在显著差异,第1组与其他两组之间也存在此类差异。

结论

中性粒细胞可能不是结肠炎氧化过程的唯一原因,这也使得皮质类固醇在治疗该疾病中的有效性存疑。

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