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一种海洋绿藻,通过NF-κB/Nrf2/SIRT1信号通路减轻二硝基苯磺酸诱导的结肠炎损伤。

a Marine Green Alga, Attenuates DNBS-Induced Colitis Damage via NF-κB/Nrf2/SIRT1 Signaling Pathways.

作者信息

Ardizzone Alessio, Filippone Alessia, Mannino Deborah, Scuderi Sarah Adriana, Casili Giovanna, Lanza Marika, Cucinotta Laura, Campolo Michela, Esposito Emanuela

机构信息

Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, Viale Ferdinando Stagno D'Alcontres, 31-98166 Messina, Italy.

出版信息

J Clin Med. 2022 Jul 25;11(15):4301. doi: 10.3390/jcm11154301.

DOI:10.3390/jcm11154301
PMID:35893393
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9331369/
Abstract

Inflammatory bowel diseases (IBD) including Crohn's disease (CD) and ulcerative colitis (UC) represent gastrointestinal (GI) disorders associated with varied responses to microbial and environmental agents. Natural compounds have been suggested as a valid approach to the management of various GI diseases, particularly the green alga , belonging to the family, which showed powerful biological properties. Here, we aimed to evaluate the effect and the mechanism of treatments in a murine model of DNBS-induced colitis. Colitis was induced by DNBS intrarectal installation (4 mg in 100 μL of 50% ethanol), while treatments (doses of 10, 50 and 100 mg/kg) were administered orally daily. , at the higher doses of 50 and 100 mg/kg, significantly reduced tissue damage DNBS-induced and the consequent inflammatory cascade via NF-κB inhibition. Furthermore, we demonstrated, for the first time, action on the SIRT1/Nrf2 axis, enhancing antioxidant response and the modulation of the apoptosis pathway colitis-induced, regulating the expression of p53, Bax, Bcl-2, and Caspases. Taken together, could be considered a valid approach for counteracting and blocking the progression of IBDs through modulation of the NF-κB/SIRT1/Nrf2 axis.

摘要

炎症性肠病(IBD)包括克罗恩病(CD)和溃疡性结肠炎(UC),是与对微生物和环境因子的不同反应相关的胃肠道(GI)疾病。天然化合物已被认为是治疗各种胃肠道疾病的有效方法,特别是属于 科的绿藻,其具有强大的生物学特性。在此,我们旨在评估 治疗在二硝基苯磺酸(DNBS)诱导的小鼠结肠炎模型中的作用及机制。通过直肠内注入DNBS(4 mg溶于100 μL 50%乙醇中)诱导结肠炎,而 治疗(剂量为10、50和100 mg/kg)每天经口给药。在50和100 mg/kg的较高剂量下, 通过抑制NF-κB显著减轻了DNBS诱导的组织损伤及随之而来的炎症级联反应。此外,我们首次证明了 对SIRT1/Nrf2轴的作用,增强了抗氧化反应并调节了结肠炎诱导的凋亡途径,调控了p53、Bax、Bcl-2和半胱天冬酶的表达。综上所述, 通过调节NF-κB/SIRT1/Nrf2轴,可能是对抗和阻止IBD进展的有效方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/512666aa9f59/jcm-11-04301-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/f7545ce574f2/jcm-11-04301-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/57ec57deef19/jcm-11-04301-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/c6a02ca0c63c/jcm-11-04301-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/dabde075c3e2/jcm-11-04301-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/dfc94018eec1/jcm-11-04301-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/ab6076cd4f31/jcm-11-04301-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/512666aa9f59/jcm-11-04301-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/f7545ce574f2/jcm-11-04301-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/57ec57deef19/jcm-11-04301-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/c6a02ca0c63c/jcm-11-04301-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/dabde075c3e2/jcm-11-04301-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/dfc94018eec1/jcm-11-04301-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/ab6076cd4f31/jcm-11-04301-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ee7/9331369/512666aa9f59/jcm-11-04301-g007.jpg

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