Hypoxia Augments Cerebral Inflammation in a Dextran Sulfate Sodium-Induced Colitis Mouse Model.
Hypoxia Augments Cerebral Inflammation in a Dextran Sulfate Sodium-Induced Colitis Mouse Model.
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缺氧加剧右旋糖酐硫酸钠诱导的结肠炎小鼠模型的脑炎症
DOI:
10.3389/fncel.2020.611764
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发表时间:
2020
影响因子:
5.3
通讯作者:
Zhu L
中科院分区:
文献类型:
--
作者:
Han Y;Ding L;Cheng X;Zhao M;Zhao T;Guo L;Li X;Geng Y;Fan M;Liao H;Zhu L
The importance of hypoxia in the pathophysiology of inflammatory bowel disease (IBD) is increasingly being realized; also, hypoxia seems to be an important accelerator of brain inflammation, as has been reported by our group and others. IBD is a chronic intestinal disorder that leads to the development of inflammation, which is related to brain dysfunction. However, no studies have reported whether hypoxia is associated with IBD-induced neuroinflammation. Therefore, the objective of the present study was to determine whether hypoxia augments cerebral inflammation in a DSS-induced colitis mouse model. The mouse model was developed using 3% DSS for five days combined with exposure to hypoxic conditions (6,000 m) for two days. Mice were randomly divided into four groups: control group, DSS group, hypoxia group, and DSS plus hypoxia group. The results demonstrated that DSS combined with hypoxia resulted in up-regulation of colonic and plasmatic proinflammatory cytokines. Meanwhile, DSS plus hypoxia increased expression of Iba1, which is a marker of activated microglia, accompanied by increased expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the brain. Moreover, the expression of tight junction proteins, such as zonula occludens-1 (ZO-1), occludin, and claudin-5, was markedly downregulated. The current study provides new insight into how hypoxia exposure induces excessive inflammatory responses andpathophysiological consequences in the brain in a DSS-induced colitis model.
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DOI:
10.1155/2016/3475356
发表时间:
2016
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
作者:
da Silva LM;Farias JA;Boeing T;Somensi LB;Beber AP;Cury BJ;Santin JR;Faloni de Andrade S
通讯作者:
Faloni de Andrade S
影响因子:
29.4
作者:
Shah, Yatrik M.;Ito, Shinji;Gonzalez, Frank J.
通讯作者:
Gonzalez, Frank J.
影响因子:
3.1
作者:
Gonçalves A;Ambrósio AF;Fernandes R
通讯作者:
Fernandes R
影响因子:
5.3
作者:
Kelly JR;Kennedy PJ;Cryan JF;Dinan TG;Clarke G;Hyland NP
通讯作者:
Hyland NP
影响因子:
2.8
作者:
Blengio, Fabiola;Raggi, Federica;Bosco, Maria Carla
通讯作者:
Bosco, Maria Carla