Lipoxin A 4 inhibited the activation of hepatic stellate cells -T6 cells by modulating profibrotic cytokines and NF-κB signaling pathway.
Autor: | Zhang T; Department of Pathophysiology, Medical College of Nanchang University, Nanchang, 330006, China., Hao H; Department of Pathology, Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China., Zhou ZQ; The First Clinical Medical College, Nanchang University, Nanchang, 330006, China., Zeng T; Medical college, Jingchu University of Technology, Jingmen, Hubei 448000, China., Zhang JM; Department of Pathophysiology, Medical College of Nanchang University, Nanchang, 330006, China., Zhou XY; Department of Pathophysiology, Medical College of Nanchang University, Nanchang, 330006, China; Jiangxi Province Key Laboratory of Tumor Etiology and Molecular Pathology, Nanchang, 330006, China. Electronic address: zhouxiaoyan@ncu.edu.cn. |
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Jazyk: | angličtina |
Zdroj: | Prostaglandins & other lipid mediators [Prostaglandins Other Lipid Mediat] 2020 Feb; Vol. 146, pp. 106380. Date of Electronic Publication: 2019 Nov 04. |
DOI: | 10.1016/j.prostaglandins.2019.106380 |
Abstrakt: | Background: The deposition of extracellular matrix (ECM) during hepatic fibrosis is an intermediate process in the progression of multiple chronic liver diseases to cirrhosis. Because activated hepatic stellate cells (HSCs) are the main source of ECM, HSCs activation is the central link in the formation of liver fibrosis. It was reported that the analogs of lipoxin A Methods: Rat HSC-T6 cells were activated by LPS and treated with LXA Results: (1) LPS activated HSC-T6 cells and up-regulated α-SMA, but LXA Conclusion: LXA (Copyright © 2019 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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