Published April 13, 2012 | Version v1
Journal article

Real-time monitoring of inflammation status in 3T3-L1 adipocytes possessing a secretory Gaussia luciferase gene under the control of nuclear factor-kappa B response element

  • 1. Department of Life Sciences, Graduate School of Bioresources, Mie University, Tsu 514-8507 (Japan)

Description

Highlights: ► Inflammation status in adipocytes can be monitored by the new assay system. ► Only an aliquot of conditioned medium is required without cell lysis. ► Inflammation-attenuating compounds can be screened more conveniently. -- Abstract: We have established 3T3-L1 cells possessing a secretory Gaussia luciferase (GLuc) gene under the control of nuclear factor-kappa B (NF-κB) response element. The 3T3-L1 cells named 3T3-L1-NF-κB-RE-GLuc could differentiate into adipocyte as comparably as parental 3T3-L1 cells. Inflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β induced GLuc secretion of 3T3-L1-NF-κB-RE-GLuc adipocytes in a concentration- and time-dependent manner. GLuc secretion of 3T3-L1-NF-κB-RE-GLuc adipocytes was also induced when cultured with RAW264.7 macrophages and was dramatically enhanced by lipopolysaccharide (LPS)-activated macrophages. An NF-κB activation inhibitor BAY-11-7085 and an antioxidant N-acetyl cysteine significantly suppressed GLuc secretion induced by macrophages. Finally, we found that rosemary-derived carnosic acid strongly suppressed GLuc secretion induced by macrophages and on the contrary up-regulated adiponectin secretion. Collectively, by using 3T3-L1-NF-κB-RE-GLuc adipocytes, inflammation status can be monitored in real time and inflammation-attenuating compounds can be screened more conveniently.

Availability note (English)

Available from http://dx.doi.org/10.1016/j.bbrc.2012.03.049

Additional details

Identifiers

DOI
10.1016/j.bbrc.2012.03.049;
PII
S0006-291X(12)00496-2;

Publishing Information

Journal Title
Biochemical and Biophysical Research Communications
Journal Volume
420
Journal Issue
3
Journal Page Range
p. 623-627
ISSN
0006-291X
CODEN
BBRCA9

Optional Information

Copyright
Copyright (c) 2012 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.