Metformin Inhibits Advanced Glycation End Products-Induced Inflammatory Response in Murine Macrophages Partly through AMPK Activation and RAGE/NFκB Pathway Suppression

Figure 5

Metformin’s inhibition on AGEs-induced inflammatory response is AMPK dependent. BMDMs were divided into 4 groups: control, AGEs, AGEs + MET, and AGEs + MET + CC group. In AGEs group, cells were cultured with AGEs at 200 mg/L for 60 min; in AGEs + MET group, cells were pretreated with metformin for 60 min and then cultured with AGEs at 200 mg/L for 60 min; in AGEs + MET + C-C group, cells were pretreated with Compound C, an AMPK inhibitor, at 5 μM for 60 min, and then they were treated with metformin at 2.0 μM for 60 min followed by AGEs at 200 mg/L for 60 min; in control group, cells were cultured with BSA at 200 mg/L for 60 min. RNA then was extracted, and mRNA levels of IL-1β (a), IL-6 (b), TNF-α (c), and IL-10 (d) were measured by real-time PCR. Bar graphs represent the results () of three independent experiments. One-way ANOVA was applied and all the overall ANOVA was significant. ; ; ; and when compared between selected groups.

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