interleukin-8 and candesartan

Several proinflammatory cytokines including IL-6 and IL-8 are produced by human adipocytes, but it is still unclear how this process is regulated. Angiotensin (Ang) II, which is also produced by adipocytes, might play a role as a regulator. In the present study, we investigated the effect of Ang II on the production of IL-6 and IL-8 in in vitro differentiated human adipocytes.. Isolation of preadipocytes and differentiation of these cells into adipocytes, Real-time quantitative reverse-transcriptase polymerase chain reaction, Western-blot, enzyme-linked immunosorbent assay, and electromobility shift assay. Ang II-stimulated IL-6 and IL-8 mRNA expression and protein release in a time- and concentration-dependent way. This action of Ang II was completely blocked by the NF-kappaB-blocker Bay 117082 and the AT1 blocker candesartan, but only partially by the AT2-blocker PD 123 319. Incubation of adipocytes with Ang II resulted in an increased phosphorylation of the p65 subunit of NF-kappaB and an increased translocation of NF-kappaB to the nucleus.. Ang II stimulates IL-6 and IL-8 production and release from human adipocytes by a NF-kappaB-dependent pathway. This proinflammatory action of Ang II seems to be mediated by the AT1 and less by the AT2 receptor subtype.

Topics: Adipocytes; Adult; Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Angiotensin II Type 2 Receptor Blockers; Benzimidazoles; Biphenyl Compounds; Cells, Cultured; Electrophoretic Mobility Shift Assay; Female; Humans; Imidazoles; Inflammation; Interleukin-6; Interleukin-8; NF-kappa B; Nitriles; Phosphorylation; Protein Processing, Post-Translational; Protein Transport; Pyridines; Receptor, Angiotensin, Type 1; RNA, Messenger; Sulfones; Tetrazoles; Transcription Factor RelA; Transcriptional Activation