Sodium Butyrate Protects Against Intestinal Oxidative Damage and Neuroinflammation in the Prefrontal Cortex of Ulcerative Colitis Mice Model

神经炎症 丁酸盐 溃疡性结肠炎 氧化应激 丁酸钠 氧化损伤 炎症性肠病 结肠炎 前额叶皮质 氧化磷酸化 炎症 内科学 化学 医学 心理学 生物化学 神经科学 疾病 发酵 基因 认知
作者
Alexandre Kléber Silveira,Henrique Mautone Gomes,Nicole Thais. Fröhlich,Luana dos Reis Possa,Lucas Santos,Flávio Gabriel Carazza Kessler,Alberto Martins,Matheus Scarpatto Rodrigues,Jade de Oliveira,Natália Duarte do Nascimento,Dienifer Hermann Sirena,Ana Helena da Rosa Paz,Daniel Pens Gelain,José Cláudio Fonseca Moreira
出处
期刊:Immunological Investigations [Taylor & Francis]
卷期号:52 (7): 796-814 被引量:9
标识
DOI:10.1080/08820139.2023.2244967
摘要

Inflammatory bowel diseases (IBD) cause increased inflammatory signalling and oxidative damage. IBDs are correlated with an increased incidence of brain-related disorders suggesting that the gut-brain-axis exerts a pivotal role in IBD. Butyrate is one of the main microbial metabolites in the colon, and it can cross the blood-brain barrier, directly affecting the brain. We induced ulcerative colitis (UC) in mice utilizing dextran sodium sulfate (DSS) in the drinking water for 7 days. Animals were divided into four groups, receiving water or DSS and treated with saline or 0,066 g/kg of Sodium Butyrate for 7 days. We also used an integrative approach, combining bioinformatics functional network and experimental strategies to understand how butyrate may affect UC. Butyrate was able to attenuate colitis severity and intestinal inflammation. Butyrate protected the colon against oxidative damage in UC and protected the prefrontal cortex from neuroinflammation observed in DSS group. Immunocontent of tight junction proteins Claudin-5 and Occludin were reduced in colon of DSS group mice and butyrate was able to restore to control levels. Occludin and Claudin-5 decrease in DSS group indicate that an intestinal barrier disruption may lead to the increased influx of gut-derived molecules, causing neuroinflammation in the prefrontal cortex, observed by increased IBA-1 marker. The probable protection mechanism of butyrate treatment occurs through NRF2 through Nrf2 and HIF-1α activation and consequent activation of catalase and superoxide dismutase. Our data suggest that systemic inflammation associated with intestinal barrier disruption in UC leads to neuroinflammation in the prefrontal cortex, which was atenuated by butyrate.
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