Interaction between NADPH-oxidase and Rho-kinase in angiotensin II-induced microglial activation

摘要: Previous studies have shown that the brain renin-angiotensin system may play a major role, via angiotensin type 1 (AT1) receptors, in regulation of neuroinflammation, oxidative stress and progression dopaminergic degeneration. Angiotensin-induced activation microglial nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase complex Rho-kinase are particularly important this respect. However, it is not known whether crosstalk between NADPH-oxidase leads to activation. In present study, we found that, substantia nigra rats, was involved angiotensin-induced activation, which, turn, N9 cell line primary cultures, signaling occurred positive feedback fashion during superoxide generation led NF-кB translocation p38 mitogen-activated protein kinase. Moreover, NF-кB, upregulated AT1 receptor expression cells through feed-forward mechanism. pathways be responsible for components response, such as changes involving motility phagocytosis, superoxide, release inflammatory cytokines. The results show both linked by common mechanism constitute basic means coordinating response.