Table of Contents
ISRN Endocrinology
Volume 2012, Article ID 237613, 8 pages
http://dx.doi.org/10.5402/2012/237613
Research Article

Octanoylated Ghrelin Inhibits the Activation of the Palmitic Acid-Induced TLR4/NF- B Signaling Pathway in THP-1 Macrophages

Diabetes Center, 2nd Xiangya Hospital, Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology of Ministry of Education, Central South University, 139 Renmin-Zhong Road, Hunan, Changsha 410011, China

Received 7 October 2012; Accepted 24 October 2012

Academic Editors: J.-B. Corcuff and C. Fürnsinn

Copyright © 2012 S. P. Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

To investigate the effect of acylated ghrelin on the activation of TLR4/NF-κB signaling pathway induced by palmitic acid in human monocyte-derived (THP-1) macrophages, THP-1 macrophages were cultured for 12 h by palmitic acid with various concentrations. The THP-1 macrophages was pretreated by acylated ghrelin at different doses for 4 h before cultivated by palmitic acid (200 μmol/L) for 12 h. We observed the level of TLR4, NF-κB p65 phosphorylation in THP-1 macrophages and TNF-α, IL-1β in culture supernatant. TLR4 mRNA was measured by real-time PCR. TLR4 protein and NF-κB p65 phosphorylation was measured by western blotting. The expression of TNF-α and IL-1β was detected by ELISA. Compared to the THP-1 macrophages without palmitic acid, the level of TLR4 mRNA protein and NF-κB p65 phosphorylation and the expression of TNF-α and IL-1β increased after treatment by palmitic acid in a dose-dependent fashion ( ). Compared to the THP-1 macrophages with palmitic acid (200 μmol/L), the level of the pervious substances decreased after preadministration by acylated ghrelin in a dose-dependent fashion. So, we make a conclusion that acylated ghrelin can regulate the activation of TLR4/NF-κB signaling pathway and inhibit the release of inflammatory cytokines in THP-1 macrophages which are stimulated by palmitic acid in a dose-dependent fashion.