= 29.6 and 1.41 µg/mL, respectively), but not AGE-2. The secretion of IL-6, TNF-α, and IL-1β was also suppressed by AGE-1 in a dose-dependent manner, and inducible nitric oxide synthase and cyclooxygenase-2 mRNA, and protein expression decreased with AGE-1 treatment. Furthermore, AGE-1 attenuated the phosphorylation of the extracellular signal-regulated kinase, p38, and c-Jun terminal kinase in lipopolysaccharide-induced RAW264.7 cells. These results suggested that compound AGE-1 may have significant effects on inflammatory factors and could potentially be used as an antiinflammatory therapeutic agent.
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Kim et al. (2016) studied this question.
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