Author:
Laribi-Habchi H,Yasmine L,Zineb S,Boucherit A,Kenza A
Abstract
Purpose: Colitis is a widespread inflammatory bowel disease with heterogeneous etiology (genetic and immunological). It is treated with drugs such as steroidal and non-steroidal anti-inflammatory that, in the long term, can cause side effects. For this reason, the exploitation of natural resources to combat this type of disease is the concern of researchers. The purpose of our study was to evaluate the anti-colitis (anti-inflammatory) effect of β-Chitosane induced in albino mice by acetic acid (5%). Methods: Mices were separated into six groups: the witness (untreated and not ulcerated), negative control group (ulcerated and untreated), the positive control ulcerated and treated with the Dexaméthasone® (1 mg/kg), and test groups ulcerated and treated with different doses of β-Chitosane (0.5 g/ kg; 0.75 g/ kg and 1 g/ kg) for the entire treatment estimated to six-days. β-Chitosane efficacy was evaluated by macroscopic and microscopic scores. Results: The clinical scores showed that β-Chitosane with a dose of 1 g/kg for the entire treatment significantly reduced the damage caused by acetic acid with a score of (3.41 ± 1.45) compared to those of the positive control which reduced less the inflammation (6.26 ± 1.23). The histological study of the colons was able to validate the effect of β-Chitosane by decreasing neutrophil infiltration and ulceration in the colon as well as by structural recovery of the mucosa. Conclusion: These results provide evidence that β-Chitosane has a protective effect against ulcerative colitis that may be due to its antioxidant, anti infectious, anti-inflammatory and healing activities.
Reference48 articles.
1. Louis, et al, Génétique et environnement dans les maladies inflammatoires chroniques de l'intestin. Renue Médicale de Liège. 2012;67: 298-304.
2. Park KT, Ehrlich OG, Allen JI, Meadows P, Szigethy EM, Henrichsen K, Kim SC, Lawton RC, Murphy SM, Regueiro M, Rubin DT, Engel-Nitz NM, Heller CA. The Cost of Inflammatory Bowel Disease: An Initiative From the Crohn's & Colitis Foundation. Inflamm Bowel Dis. 2020 Jan 1;26(1):1-10. doi: 10.1093/ibd/izz104. Erratum in: Inflamm Bowel Dis. 2020 Jun 18;26(7):1118. PMID: 31112238; PMCID: PMC7534391.
3. Frank DN, Robertson CE, Hamm CM, Kpadeh Z, Zhang T, Chen H, Zhu W, Sartor RB, Boedeker EC, Harpaz N, Pace NR, Li E. Disease phenotype and genotype are associated with shifts in intestinal-associated microbiota in inflammatory bowel diseases. Inflamm Bowel Dis. 2011 Jan;17(1):179-84. doi: 10.1002/ibd.21339. Epub 2010 Sep 13. PMID: 20839241; PMCID: PMC3834564.
4. Welcker, et al, Augmenntation de la perméabilité intestinale chez les patients atteints d'une maladie inflammatoire de l'intestin. European Journal of Medical Research. 2004;9:456-460.
5. Pizarro TT, Cominelli F. Cytokine therapy for Crohn's disease: advances in translational research. Annu Rev Med. 2007;58:433-44. doi: 10.1146/annurev.med.58.121205.100607. PMID: 17217333.