福克斯O1
医学
下调和上调
蛋白激酶B
肝损伤
炎症
PI3K/AKT/mTOR通路
流式细胞术
再灌注损伤
免疫学
癌症研究
缺血
信号转导
内科学
生物
细胞生物学
基因
生物化学
作者
Haozhen Ren,Senzhe Xia,Xue-qian Qin,Anyin Hu,Jinglin Wang
出处
期刊:Journal of clinical and translational hepatology
[Xia & He Publishing]
日期:2022-03-15
卷期号:000 (000): 000-000
被引量:6
标识
DOI:10.14218/jcth.2021.00551
摘要
Hepatic ischemic reperfusion injury (IRI) occurring during surgery seriously affects patient prognosis. The specific mechanism of IRI has not been fully elucidated. The study aim was to explore the changes of inflammatory environment, and the relationship of the Th17/Treg cell ratio and FOXO1 expression in hepatic IRI.Liver samples at different ischemic times were collected from patients and mice. The expression of inflammatory markers and FOXO1 in the liver was detected by western blotting and qPCR. Phenotypic changes of liver lymphocytes were analyzed by flow cytometry. The AKT/Stat3/FOXO1 pathway was verified by targeting AKT with GSK2141795. The role of FOXO1 in liver inflammation and changes in lymphocyte phenotype was confirmed by upregulating FOXO1 with resveratrol.Prolonged ischemic time aggravates liver injury in both humans and mouse models of hepatic IRI. IR-stress caused Th17/Treg imbalance and FOXO1 down-regulation by activating the AKT/Stat3/FOXO1 signaling pathway. Upregulation of FOXO1 reversed the Th17/Treg cytokine imbalance and altered the inflammation environment in the liver.Liver IRI induced Th17/Treg imbalance. Upregulation of FOXO1 reversed the imbalance and alleviated liver inflammation.
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