Figure 5
From: Neuroinflammation and neurologic deficits in diabetes linked to brain accumulation of amylin
Amylin deposition in the brain triggers an inflammatory response. A and B – Immunohistochemistry analysis with an ED1 antibody on brain sections from HIP rats shows possible activated microglia/macrophages (arrows). B and C – Microglia/macrophages are particularly clustering around the small blood vessels in areas positive for amylin infiltration, as shown by serial staining with amylin (C) and ED1 (B) antibodies. D – qRT-PCR was used to analyze a subset of gene expression markers [48] defining microglia as classically activated (M1) or alternatively activated (M2a/b/c). The expression of both M1 and M2 phenotypic markers are increased in the cortex of HIP rats relative to WT rats suggesting that amylin deposition activates microglia. E – The association of brain amylin pathology with neuroinflammation was tested by western blots with TNF-α, IL-6 and IL-10 antibodies. Brain protein homogenates from HIP rats show elevated pro-inflammatory cytokines TNF-α and IL-6, while the anti-inflammatory cytokine IL-10 is down-regulated. Equal loading was verified by re-probing with a monoclonal anti-β actin antibody (*P < 0.05; **P < 0.01; N = 6 animals/group).