Human Gp130/IL6ST(Interleukin-6 receptor subunit beta) ELISA Kit

The aim of the present study was to elucidate the molecular mechanisms underlying the anti-inflammatory effect of Scutellaria Radix (SR). The complementary DNA (cDNA) microarray method was used to survey the effects of SR on the changes of gene expression profile in HEK293 cells. Based on differential expression, 66 genes were selected for further analysis from 9600 candidate genes in the microarray; 23 genes were validated by RT-PCR. The broad spectrum of the differentially expressed genes, including those associated with inflammation, immune response, energy metabolism, as well as others, such as ISGF3G, IL6ST, CD98, ATP5G2, PHKG2, YB-1 and SLC7A4, indicate overall cellular response to SR treatment. Our results suggest that the anti-inflammatory effect of SR may be related to IL6ST down-expression, and over-expression of CD98. Moreover, SR-related improvement in immune response may be related to the ISGF3G over-expression. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

Background: Hepatic iron overload is common in patients who have undergone hematopoietic cell transplantation (HCT) and may predispose to peri- and post-HCT toxicity. To better reveal more molecules that might be involved in iron overload-induced liver injury, we utilized proteomics to investigate differentially expressed proteins in iron overload-induced hepatocytes vs. untreated hepatocytes. Methods and Results: HH4 hepatocytes were exposed to ferric ammonium citrate (FAC) to establish an in vitro iron overload model. Differentially expressed proteins initiated by the iron overload were studied by two-dimensional liquid chromatography tandem mass spectrometry (2D-LC-MS) analysis. We identified 93 proteins whose quantity statistically significantly changes under excess hepatocyte iron conditions. Gene Ontology (GO) analysis showed that these differentially expressed proteins in HH4 cells are involved in various biological process including endocytosis, response to wounding, di-, trivalent inorganic cation homeostasis, inflammatory response, positive regulation of cytokine production, and etc. Meanwhile, proteomics data revealed protein level of TLR2 and IL6ST significantly increased 7 times and 2.9 times, respectively, in iron overloaded HH4 cells. Our subsequent experiments detected that FAC-treated HH4 cells can activate IL6 expression through TLR2-mediated inflammatory responses via the NF-B pathway. Conclusions: In this study, we demonstrated that iron overload induced hepatocytes triggering TLR2-mediated inflammatory response via NF-B signaling pathway in HH4 cells.