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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Arhalofenate acid inhibits monosodium urate crystal-induced inflammatory responses through activation of AMP-activated protein kinase (AMPK) signaling

Fig. 5

Arhalofenate acid activated AMPK downstream targets involved in regulation of mitochondrial function and maintained mitochondrial cristae area. BMDMs were treated with arhalofenate acid (100 μM) for 1 h before stimulation with monosodium urate (MSU) crystals (0.2 mg/mL) for 1 h or 18 h in RPMI containing 1% FBS. Cell lysates prepared from 18-h treatment samples were subjected to Western blot analysis of phosphorylation (p) and expression of AMP-activated protein kinase (AMPK)α, expression of sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α), and mitochondrial transcription factor A (TFAM), and expression of thioredoxin (TRX)1, TRX2, and thioredoxin-interacting protein (TXNIP) (a). Cells from 1-h treatment were then stained with MitoSOX Red and MitoTracker Green and visualized by fluorescence microscopy (b, magnification 20×). TEM analysis was performed to examine mitochondrial cristae (the folds of inner mitochondrial membrane indicated by white arrows in c), and the cristae volume density are presented (d). Data in a and b are representative of three individual experiments. Data in c are representative of 30 cells examined for each condition. Data in d are the mean ± SEM of 30 cells. The p values represent comparisons between none and MSU crystals alone, or between MSU crystals alone and MSU crystals plus arhalofenate acid

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