维生素 D 缺乏对慢性酒精性肝损伤的影响

IF 7.1 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
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引用次数: 0

摘要

在酗酒者中发现了维生素 D 缺乏症(VDD)。然而,人们对维生素 D 缺乏对酒精性肝病的影响知之甚少,其分子机制也仍不清楚。本研究旨在评估酒精性脂肪肝(AFLD)患者是否缺乏维生素D,以及维生素DD对小鼠慢性酒精性肝损伤的影响和可能的分子机制。我们的研究结果发现,酒精性脂肪肝患者体内的 25- 羟维生素 D [25(OH)D] 浓度较低。进一步分析发现,25(OH)D 是 AFLD 患者的保护因子。小鼠实验表明,VDD 可改变肠道微生物群的组成,下调肠道紧密连接蛋白 Occludin 和 E-cadherin 的蛋白水平,上调肝脏和结肠组织中炎症细胞因子(tnf-α、il-1β、il-6、il-8、cl2、il-10)的表达。酒精性肝损伤小鼠的 p65、P-IκB、P-p65 蛋白水平进一步升高。总之,VDD 通过激活 NF-κB 信号通路加重慢性酒精性肝损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Effects of vitamin D deficiency on chronic alcoholic liver injury

Effects of vitamin D deficiency on chronic alcoholic liver injury

Vitamin D deficiency (VDD) has been found among alcoholics. However, little is known about the effect of VDD on alcoholic liver disease and the molecular mechanisms remain unclear. The aim of the current study was to evaluate whether vitamin D was deficient among patients with alcoholic fatty liver disease (AFLD) and the effect of VDD on chronic alcoholic liver injury and possible molecular mechanisms in mice. Our results found that lower 25-hydroxyvitamin D [25(OH)D] concentrations in patients with AFLD. And further analysis found that 25(OH)D is a protective factor in patients with AFLD. Mice experiments indicated that VDD can alter the composition of gut microbiota, down-regulate the protein levels of intestinal tight junction protein Occludin and E-cadherin, up-regulate the expression of inflammatory cytokines (tnf-α, il-1β, il-6, il-8, ccl2, il-10) in liver and colon tissue. And further exacerbated the protein levels of p65,P-IκB,P-p65 in alcoholic liver injury mice. In conclusion, VDD aggravates chronic alcoholic liver injury by activating NF-κB signaling pathway.

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来源期刊
Free Radical Biology and Medicine
Free Radical Biology and Medicine 医学-内分泌学与代谢
CiteScore
14.00
自引率
4.10%
发文量
850
审稿时长
22 days
期刊介绍: Free Radical Biology and Medicine is a leading journal in the field of redox biology, which is the study of the role of reactive oxygen species (ROS) and other oxidizing agents in biological systems. The journal serves as a premier forum for publishing innovative and groundbreaking research that explores the redox biology of health and disease, covering a wide range of topics and disciplines. Free Radical Biology and Medicine also commissions Special Issues that highlight recent advances in both basic and clinical research, with a particular emphasis on the mechanisms underlying altered metabolism and redox signaling. These Special Issues aim to provide a focused platform for the latest research in the field, fostering collaboration and knowledge exchange among researchers and clinicians.
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