Dual role of melatonin as an anti-colitis and anti-extra intestinal alterations against acetic acid-induced colitis model in rats

被引:21
作者
Ahmed, Osama [1 ]
Farid, Alyaa [1 ]
Elamir, Azza [1 ]
机构
[1] Cairo Univ, Fac Sci, Zool Dept, Giza 12613, Egypt
关键词
INFLAMMATORY-BOWEL-DISEASE; DINITROBENZENE SULFONIC-ACID; ULCERATIVE-COLITIS; LIPID-PEROXIDATION; OXIDATIVE STRESS; EXPRESSION; CYTOKINE; SEVERITY; COX-2;
D O I
10.1038/s41598-022-10400-y
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The available ulcerative colitis drugs exhibit limited outcomes and adverse side effects. Therefore, our study aimed to investigate the therapeutic efficacy of melatonin in acetic acid (AA)-induced colitis to establish a possible treatment for colitis and its impacts on vital organs. Following colitis induction (2 ml 5% AA, rectally), rats were orally received melatonin (5 mg/kg) once per day for 6 days after colitis induction. Then, histopathological examination of colon, kidney, liver, and spleen was conducted, interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH), and total antioxidant capacity (TAC) levels were assessed in colon tissue. Colitis induction in untreated rats caused necrotic effects in colon tissues, a significant increase in colonic IL-1 beta, TNF-alpha, MPO, and MDA levels, and a remarkable decrease in GSH and TAC levels in colon tissue in comparison to the control group. Meanwhile, melatonin treatment reversed these parameters by improving the microscopic and macroscopic colitis features and extra-intestinal (kidney, liver, and spleen) changes in all treated rats compared to the colitis control group. These results denote a reduction in colitis severity due to the anti-inflammatory and anti-oxidative effects of melatonin and its positive impact on the vital organs.
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页数:12
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共 53 条
[1]   Taurine loaded chitosan-pectin nanoparticle shows curative effect against acetic acid-induced colitis in rats [J].
Ahmed, Osama ;
Abdel-Halim, Mohammad ;
Farid, Alyaa ;
Elamir, Azza .
CHEMICO-BIOLOGICAL INTERACTIONS, 2022, 351
[2]   Roles of Dietary Amino Acids and Their Metabolites in Pathogenesis of Inflammatory Bowel Disease [J].
Bao, Xianying ;
Feng, Zemeng ;
Yao, Jiming ;
Li, Tiejun ;
Yin, Yulong .
MEDIATORS OF INFLAMMATION, 2017, 2017
[3]   Cytokines in inflammatory bowel disease [J].
Beck, PL ;
Wallace, JL .
MEDIATORS OF INFLAMMATION, 1997, 6 (02) :95-103
[4]  
Berg Rodney D., 1995, Trends in Microbiology, V3, P149, DOI 10.1016/S0966-842X(00)88906-4
[5]   The immune response in inflammatory bowel disease [J].
Brown, Steven J. ;
Mayer, Lloyd .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 2007, 102 (09) :2058-2069
[6]  
Bubenik GA, 2008, J PHYSIOL PHARMACOL, V59, P33
[7]   Guidelines for the management of inflammatory bowel disease in adults [J].
Carter, MJ ;
Lobo, AJ ;
Travis, SPL .
GUT, 2004, 53 :v1-v16
[8]   Myeloperoxidase in the inflamed colon: A novel target for treating inflammatory bowel disease [J].
Chami, Belal ;
Martin, Nathan J. J. ;
Dennis, Joanne M. ;
Witting, Paul K. .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2018, 645 :61-71
[9]   Cytokine Networks and T-Cell Subsets in Inflammatory Bowel Diseases [J].
Chen, Mei Lan ;
Sundrud, Mark S. .
INFLAMMATORY BOWEL DISEASES, 2016, 22 (05) :1157-1167
[10]   IL-1β mediates chronic intestinal inflammation by promoting the accumulation of IL-17A secreting innate lymphoid cells and CD4+ Th17 cells [J].
Coccia, Margherita ;
Harrison, Oliver J. ;
Schiering, Chris ;
Asquith, Mark J. ;
Becher, Burkhard ;
Powrie, Fiona ;
Maloy, Kevin J. .
JOURNAL OF EXPERIMENTAL MEDICINE, 2012, 209 (09) :1595-1609