Skip to main content
. 2019 Oct 1;8(10):1185. doi: 10.3390/cells8101185

Figure 3.

Figure 3

Role of adenosine monophosphate (AMP)-activated protein kinase (AMPK) in potentiating Ptgs2 expression by mitochondrial inhibitors. (A) The mRNA expression of Ptgs2 in astrocytes treated with IL-1α for 3 hours in the absence or presence of mito-TEMPO, antimycin, and oligomycin, as indicated. (B,C) Intracellular adenosine triphosphate (ATP) (B) and AMP (C) levels in astrocytes treated with rotenone, antimycin, and oligomycin for 1 hour. (D) Western blot analysis of AMPK and acetyl-CoA carboxylase (ACC) phosphorylation in astrocytes treated for 1 hour with IL-1α in the absence or presence of rotenone, oligomycin, and antimycin, as indicated. (E) Ptgs2 mRNA expression in astrocytes treated with IL-1α, phenformin, and A-769662 for 3 hours. (F) The mRNA expression of Ptgs2 and Prkaa1 in astrocytes transfected with control or Prkaa1 siRNAs for 96 hours and treated for 3 hours with IL-1α in the presence or absence of oligomycin as indicated. (G) Western blot analysis of Ptgs2 and Prkaa1 expression in astrocytes transfected with control or Prkaa1 siRNAs for 96 hours and treated for 4 hours with IL-1α in the presence or absence of oligomycin, as indicated. (H) The mRNA expression of Ptgs2 in astrocytes treated with IL-1α and phenformin for 1 hour followed by actinomycin D for indicated times. Note: *, p < 0.05 vs. untreated (B,C), IL-1α (E), or vs. siControl for each treatment condition (F). Data represent mean values ± SE of 3 or 4 independent experiments.