Rosiglitazone Suppresses Renal Crystal Deposition by Ameliorating Tubular Injury Resulted from Oxidative Stress and Inflammatory Response via Promoting the Nrf2/HO-1 Pathway and Shifting Macrophage Polarization

<div>ROSI declined COM-stimulated M1Mp polarization and crystal adhesion and promoted M2Mp polarization in vitro. (a) Fluorescence immunohistochemical distribution of Arg1 (green) and iNOS (red) in THP-1 cells with the stimulus of COM or ROSI (1 <i>μ</i>M) or GW9662 (10 <i>μ</i>M) (arrows). (b) Evaluation of mean fluorescence intensity (MFI) of Arg1 and iNOS. (c) ELISA. The expression levels of IL-4, IL-10, IL-6, and TNF-<i>α</i>. (d) Crystal adhesion assay. COM crystal adhesion to HK-2 cells was observed (arrows). 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Oxidative Medicine and Cellular Longevity

fig6

Figure 6

Figure 6: Rosiglitazone Suppresses Renal Crystal Deposition by Ameliorating Tubular Injury Resulted from Oxidative Stress and Inflammatory Response via Promoting the Nrf2/HO-1 Pathway and Shifting Macrophage Polarization 

Figure 6 | Rosiglitazone Suppresses Renal Crystal Deposition by Ameliorating Tubular Injury Resulted from Oxidative Stress and Inflammatory Response via Promoting the Nrf2/HO-1 Pathway and Shifting Macrophage Polarization 