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褪黑素在大鼠乙酸诱导的结肠炎模型中作为抗结肠炎和抗肠外改变的双重作用。

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

作者信息

Ahmed Osama, Farid Alyaa, Elamir Azza

机构信息

Zoology Department, Faculty of Science, Cairo University, Giza, 12613, Egypt.

出版信息

Sci Rep. 2022 Apr 15;12(1):6344. doi: 10.1038/s41598-022-10400-y.

DOI:10.1038/s41598-022-10400-y
PMID:35428860
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9012815/
Abstract

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-1β), tumor necrosis factor-alpha (TNF-α), 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-1β, TNF-α, 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.

摘要

现有的溃疡性结肠炎药物疗效有限且有不良副作用。因此,我们的研究旨在调查褪黑素对乙酸(AA)诱导的结肠炎的治疗效果,以确立一种可能的结肠炎治疗方法及其对重要器官的影响。在诱导结肠炎(经直肠给予2毫升5%的AA)后,大鼠在诱导结肠炎后每天口服一次褪黑素(5毫克/千克),持续6天。然后,对结肠、肾脏、肝脏和脾脏进行组织病理学检查,并评估结肠组织中的白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、髓过氧化物酶(MPO)、丙二醛(MDA)、谷胱甘肽(GSH)和总抗氧化能力(TAC)水平。与对照组相比,未治疗大鼠的结肠炎诱导导致结肠组织出现坏死效应,结肠IL-1β、TNF-α、MPO和MDA水平显著升高,结肠组织中的GSH和TAC水平显著降低。同时,与结肠炎对照组相比,褪黑素治疗通过改善所有治疗大鼠的微观和宏观结肠炎特征以及肠外(肾脏、肝脏和脾脏)变化,逆转了这些参数。这些结果表明,由于褪黑素的抗炎和抗氧化作用及其对重要器官的积极影响,结肠炎的严重程度有所降低。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5102/9012815/1146953161e8/41598_2022_10400_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5102/9012815/1146953161e8/41598_2022_10400_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5102/9012815/efa1abca9a89/41598_2022_10400_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5102/9012815/fd05d3745a5d/41598_2022_10400_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5102/9012815/24a10f61c421/41598_2022_10400_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5102/9012815/d8cfc2d2ab1a/41598_2022_10400_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5102/9012815/cd85444ef6eb/41598_2022_10400_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5102/9012815/e396127b0f0d/41598_2022_10400_Fig6_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5102/9012815/1146953161e8/41598_2022_10400_Fig8_HTML.jpg

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