Angiotensin II stimulates MCP-1 production in rat glomerular endothelial cells via NAD(P)H oxidase-dependent nuclear factor-kappa B signaling.

摘要: Angiotensin II (Ang II) plays a crucial role in the pathogenesis of renal diseases. The objective present study was to investigate possible inflammatory effect Ang on glomerular endothelial cells and underlying mechanism. We isolated characterized primary cultures rat (GECs) observed that induced synthesis monocyte chemoattractant protein-1 (MCP-1) GECs as demonstrated by Western blot. stimulation, at concentrations ranging from 0.1 10 microm, rapid increase generation reactive oxygen species indicated laser fluoroscopy. level p47phox protein, an NAD(P)H oxidase subunit, also increased treatment. These effects were all reduced diphenyleneiodonium (1.0 microm), inhibitor. stimulation promoted activation nuclear factor-kappa B (NF-kappaB). Telmisartan AT1 receptor blocker, blocked GECs. data suggest inhibition oxidase-dependent NF-kappaB signaling reduces MCP-1 production II. This may provide mechanistic basis for benefits selective blockade dealing with chronic disease.