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. 2019 Feb 28;20(5):1050. doi: 10.3390/ijms20051050

Figure 1.

Figure 1

Proposed mechanisms of liraglutide activity; ↓ = reduction, ↑ = increase, p-p38 = phosphorylated p38, JNK-c = jun-NH2-terminal kinase, AKT = protein kinase B, ERK = extracellular signal-adjusted kinases, Bcl-2 = B-cell lymphoma 2, Bax = bcl-2-like protein 4, Bcl-xl = B-cell lymphoma-extra-large, Bad = Bcl-2-associated death promoter, NFκB = Nuclear Factor-kappaB, ICAM-1 = Intercellular Adhesion Molecule 1 Nrf2/HO-1-nuclear factor erythroid 2-related factor/heme oxygenase-1, MDA = malondialdehyde, GSH = glutathione, SOD = superoxide dismutase, MPO = myeloperoxidase, ROS = Reactive oxygen species, eNOS = endothelial nitric oxide synthase, ET-1 = Endothelin-1, eNOS = endothelial nitric oxide synthase, IL-6 = Interleukin-6, ACAT-1 = acyl-CoA: cholesterol acyltransferase 1, IDE = insulin degrading enzyme, Aβ = amyloid β, NSCs = neuronal stem cells, cAMP/PKA = cyclic adenosine monophosphate/phosphorylase kinase A.