Figure 10. 5‐Aminoimidazole‐4‐carboxamide 1‐β‐D‐ribofuranoside (AICAR) inhibits the emergence of a systemic inflammatory response syndrome–associated inflammatory phenotype in cardiac myocytes.

Cardiac myocytes were preincubated with AICAR (1 mmol/L) or vehicle (H₂O) for 2 hours before stimulation with lipopolysaccharide (1 mg/mL) for 1 hour. A, Concentration of TNF‐α (tumor necrosis factor α) in culture supernatants and (B) content of lactate dehydrogenase (LDH) in culture supernatants was quantified by ELISA (n=7) and activity assay (n=7), respectively. Cardiac myocytes were preincubated with AICAR (1 mmol/L) or vehicle (H₂O) for 2 hours before stimulation with lipopolysaccharide (1 mg/mL) for 1 hour. mRNA expression of (C) the chemokine CCL2 (C‐C chemokine ligand 2), (D) the enzyme inducible nitric oxide synthase (iNOS), and (E) the cytokine IL (interleukin) 10 was measured relative to 18S ribosomal RNA (rRNA) by quantitative real‐time polymerase chain reaction (n=6). F, Phosphorylation of AMP‐activated protein kinase (AMPK) in cell lysates was analyzed by immunoblot (n=5). Upper panel: representative pictures of the resulting phosphorylated AMPK (P‐AMPK; molecular weight: 62 kDa) and AMPK (molecular weight: 62 kDa) band patterns. Lower panel: column bars indicate quantified P‐AMPK/AMPK expression ratios. Results are presented as mean+SEM. Differences of marker expression levels between experimental groups were analyzed statistically by performing the indicated pairwise comparisons.