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 suppressed CaOx-induced oxidative stress injury and promoted the Nrf2/HO-1 pathway in HK-2 cell. (a) Cellular LDH levels in HK-2 cells. (b) HK-2 cell death by flow cytometry. (c) mRNA expression levels of Nrf2, HO-1, and SOD1 in HK-2 cells by qRT-PCR. (d) The expression of PPAR<i>γ</i>, Nrf2, HO-1, and SOD1 in HK-2 cells by Western blot. (e) Detection of intracellular ROS levels by a fluorescence microscope. (f) H<sub>2</sub>O<sub>2</sub>, MDA, and GSH levels in HK-2 cells. 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Oxidative Medicine and Cellular Longevity

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Figure 4

Figure 4: 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 4 | 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 