We used casein injection in C57BL/6J mice, interleukin-1β and interleukin-6 stimulation in human hepatoblastoma cell line (HepG2) cells to induce inflammatory stress.
The present study investigated the effects of interleukin-6 (IL-6), IL-1 beta, and dexamethasone on CBG synthesis by a clone of human hepatoblastoma-derived (HepG2) cell line.
A human hepatoblastoma cell line (C3A, a subclone of HepG2/C3 that is currently being used as a surrogate liver) and human lung adenocarcinoma cells (A549) were stimulated with interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF alpha), interferon-gamma (IFN gamma), or IL-6 to determine any differences in cell type responsiveness to individual cytokines for ICAM-1 upregulation.
A 5'-flanking region (-2024 to +61) of the guinea pig liver transglutaminase gene and some 5'-deletion mutants were tested for promoter activity in human hepatoblastoma HepG2 cells treated with interleukin-6 (IL-6) by an assay of the transient expression of the chloramphenicol acetyltransferase reporter gene.
Interleukin-6 (IL-6), the main mediator of the acute phase phenomenon, increases alpha 1-antitrypsin and alpha 1-antichymotrypsin synthesis and decreases T4-binding globulin synthesis by human hepatoblastoma-derived (Hep G2) cells.
When evaluated in human hepatoblastoma-derived (Hep G2) cells exposed to different doses of the recombinant human cytokine for variable time intervals, IL-6 caused a dose- and time-dependent decrease in the secretion of [35S]methionine-labeled TBG, transthyretin (TTR), and albumin.