Regulation of HepG2 Fat Metabolism by IL1β and IL1 Receptor Antagonist
Cancer Research Journal
Volume 5, Issue 4, July 2017, Pages: 24-34
Received: Dec. 7, 2017; Accepted: Dec. 22, 2017; Published: Jan. 16, 2018
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Susmita Chandra, Department of Biotechnology, Maulana Abul Kalam Azad University of Technology, West Bengal, India
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Abstract
Non-alcoholic fatty liver disease (NAFLD) is the major cause of steatohepatitis, cirrhosis and hepatocellular carcinoma. High saturated fat rich diet is one of the known causes of NAFLD. Non-Alcoholic liver disease NAFLD is characterized by steatosis and upregulation of different proinflammatory cytokines, like caspase-1 dependant IL1β, type I IL1 receptor (IL1R1), and IL1 receptor antagonist (IL1Ra). Till date there is no proper treatment option available for NASH except management of obesity and food intake. Anti inflammatory drugs are used as a treatment option in atherosclerosis, where inflammatory response plays an important role. Keeping a similarity in mind the recombinant IL1Ra and inflammatory cytokine IL1β was tested as treatmet option for high fat condition in Palmitate treated HepG2 cells. The lipid metabolism pathways were tested with a purchased recombinant product as well as with THP1 and its macrophage extracted product. The major outcome was removal of storage fat from the cells by increasing the beta oxidation level. So the conclusion was that IL1Ra can play a major role in controlling the accumulated fatty level in liver cells.
Keywords
NAFLD, IL1β, IL1Ra, THP1-Monocyte and Macrophage
To cite this article
Susmita Chandra, Regulation of HepG2 Fat Metabolism by IL1β and IL1 Receptor Antagonist, Cancer Research Journal. Vol. 5, No. 4, 2017, pp. 24-34. doi: 10.11648/j.crj.20170504.11
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Copyright © 2017 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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