溃疡性结肠炎（UC）是一种慢性复发性炎症性肠病（IBD），其特征是结肠黏膜持续炎症。肠道屏障破坏和增渗由于氧化还原失衡、菌群失调和肠道炎症引起，导致外肠道表现（EIM）发生，对发病率和死亡率有影响。本研究旨在调查口服乙酰半胱氨酸（NAC）对二硫酸硫酸内酯（DSS）诱导结肠炎小鼠结肠、肝和肾组织的影响。雄性瑞士小鼠在结肠炎诱导前30天和期间（DSS 5％ v/v；连续7天）在饮用水中接受NAC（150mg/kg/天）。在第38天，收集结肠，肝脏和肾脏，并进行适当处理，以分析氧化应激相关指标（超氧化物歧化酶（SOD），过氧化氢酶（CAT），还原型谷胱甘肽（GSH），氧化型谷胱甘肽（GSSG），丙二醛（MDA）和过氧化氢（H2O2））以及炎症生物标志物（髓过氧化物酶（MPO），肿瘤坏死因子α（TNF-α）和白细胞介素-10（IL-10））。在结肠方面，NAC保护了组织的组织学结构，但未提高SOD反而增加了MDA和促炎效应（增加TNF-α并降低IL-10）。在肝脏方面，结肠炎引起氧化（MDA，SOD和GSH）和炎症损伤（IL-10）。NAC只增加了GSH和GSH/GSSG比率。肾脏未受结肠炎影响；然而，尽管NAC增加了CAT，GSH和GSH/GSSG比率，但促进了脂质过氧化作用（增加MDA）和促炎作用（减少IL-10）。尽管NAC具有一些有益的抗氧化作用，但在结肠，肝脏和肾脏中造成不可逆的氧化和炎症损害的负面结果表明，在诱导结肠炎模型中预防性使用该抗氧化剂是不安全的，建议进行额外研究，目前不建议将其用于治疗这种疾病的常规用途。版权所有©2023年Amylly Sanuelly da Paz Martins等。

Ulcerative colitis (UC) is a chronic and recurrent inflammatory bowel disease (IBD) characterized by continuous inflammation in the colonic mucosa. Extraintestinal manifestations (EIM) occur due to the disruption of the intestinal barrier and increased permeability caused by redox imbalance, dysbiosis, and inflammation originating from the intestine and contribute to morbidity and mortality. The aim of this study is to investigate the effects of oral N-acetylcysteine (NAC) on colonic, hepatic, and renal tissues in mice with colitis induced by dextran sulfate sodium (DSS). Male Swiss mice received NAC (150 mg/kg/day) in the drinking water for 30 days before and during (DSS 5% v/v; for 7 days) colitis induction. On the 38th day, colon, liver, and kidney were collected and adequately prepared for the analysis of oxidative stress (superoxide dismutase (SOD), catalase (CAT), glutathione reduced (GSH), glutathione oxidized (GSSG), malondialdehyde (MDA), and hydrogen peroxide (H2O2)) and inflammatory biomarkers (myeloperoxidase (MPO) -, tumor necrosis factor alpha - (TNF-α, and interleukin-10 (IL-10)). In colon, NAC protected the histological architecture. However, NAC did not level up SOD, in contrast, it increased MDA and pro-inflammatory effect (increased of TNF-α and decreased of IL-10). In liver, colitis caused both oxidative (MDA, SOD, and GSH) and inflammatory damage (IL-10). NAC was able only to increase GSH and GSH/GSSG ratio. Kidney was not affected by colitis; however, NAC despite increasing CAT, GSH, and GSH/GSSG ratio promoted lipid peroxidation (increased MDA) and pro-inflammatory action (decreased IL-10). Despite some beneficial antioxidant effects of NAC, the negative outcomes concerning irreversible oxidative and inflammatory damage in the colon, liver, and kidney confirm the nonsafety of the prophylactic use of this antioxidant in models of induced colitis, suggesting that additional studies are needed, and its use in humans not yet recommended for the therapeutic routine of this disease.Copyright © 2023 Amylly Sanuelly da Paz Martins et al.