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维生素 D 缺乏加剧慢性酒精性肝损伤小鼠肝氧化应激和炎症反应。

Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice.

机构信息

Department of Toxicology, School of Public Health, Anhui Medical University, Hefei 230032, China.

Department of Nutrition and Hygiene, School of Public Health, Anhui Medical University, Hefei 230032, China.

出版信息

Oxid Med Cell Longev. 2020 Feb 27;2020:5715893. doi: 10.1155/2020/5715893. eCollection 2020.

DOI:10.1155/2020/5715893
PMID:32184917
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7063183/
Abstract

Vitamin D deficiency has been reported in alcoholics. This study is aimed at evaluating the effects of vitamin D deficiency on chronic alcohol-induced liver injury in mice. Mice were fed with modified Lieber-DeCarli liquid diets for 6 weeks to establish an animal model of chronic alcohol-induced liver injury. In the VDD+EtOH group, mice were fed with modified diets, in which vitamin D was depleted. Vitamin D deficiency aggravated alcohol-induced liver injury. Furthermore, vitamin D deficiency aggravated hepatocyte apoptosis during alcohol-induced liver injury. Although it has a little effect on hepatic TG content, vitamin D deficiency promoted alcohol-induced hepatic GSH depletion and lipid peroxidation. Further analysis showed that vitamin D deficiency further increased alcohol-induced upregulation of hepatic inducible nitric oxide synthase (), two NADPH oxidase subunits and , and heme oxygenase- (HO-) 1. By contrast, vitamin D deficiency attenuated alcohol-induced upregulation of hepatic antioxidant enzyme genes, such as superoxide dismutase () 1 and . In addition, vitamin D deficiency significantly elevated alcohol-induced upregulation of hepatic proinflammatory cytokines and chemokines. Taken together, these results suggest that vitamin D deficiency aggravates hepatic oxidative stress and inflammation during chronic alcohol-induced liver injury.

摘要

维生素 D 缺乏症在酗酒者中已有报道。本研究旨在评估维生素 D 缺乏对慢性酒精性肝损伤的影响。通过给予改良的 Lieber-DeCarli 液体饮食 6 周，建立了慢性酒精性肝损伤的动物模型。在 VDD+EtOH 组中，给予缺乏维生素 D 的改良饮食。维生素 D 缺乏加重了酒精诱导的肝损伤。此外，维生素 D 缺乏加重了酒精性肝损伤时的肝细胞凋亡。尽管对肝 TG 含量影响较小，但维生素 D 缺乏促进了酒精诱导的肝 GSH 耗竭和脂质过氧化。进一步分析表明，维生素 D 缺乏进一步增加了酒精诱导的肝诱导型一氧化氮合酶（）、两个 NADPH 氧化酶亚基 和 以及血红素加氧酶-1（HO-1）的上调。相比之下，维生素 D 缺乏减弱了酒精诱导的肝抗氧化酶基因的上调，如超氧化物歧化酶 1（）和 。此外，维生素 D 缺乏显著增加了酒精诱导的肝促炎细胞因子和趋化因子的上调。总之，这些结果表明，维生素 D 缺乏加重了慢性酒精性肝损伤时的肝氧化应激和炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/54869461a3be/OMCL2020-5715893.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/dc292adfe5b0/OMCL2020-5715893.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/f9d62b46d5d4/OMCL2020-5715893.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/daaa288581a4/OMCL2020-5715893.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/7ea69ef958e8/OMCL2020-5715893.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/89bc533e724a/OMCL2020-5715893.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/54869461a3be/OMCL2020-5715893.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/dc292adfe5b0/OMCL2020-5715893.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/f9d62b46d5d4/OMCL2020-5715893.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/daaa288581a4/OMCL2020-5715893.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/7ea69ef958e8/OMCL2020-5715893.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/89bc533e724a/OMCL2020-5715893.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b3e/7063183/54869461a3be/OMCL2020-5715893.006.jpg

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