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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Role of endoplasmic reticulum stress in the protective effects of PPARβ/δ activation on endothelial dysfunction induced by plasma from patients with lupus

Fig. 5

Role of endoplasmic reticulum (ER)-stress in endothelial dysfunction induced by plasma from patients with systemic lupus erythematosus (SLE) and active nephritis (AN). Reactive oxygen species (ROS) production (a, b), measured by fluorescence in CM-H2DCFDA, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity (c), measured by lucigenin-enhanced chemiluminescence, measured in human umbilical cord vein endothelial cells (HUVECs) incubated in plasma from patients with SLE with AN, or in plasma from patients with antiphospholipid syndrome (APS), or healthy controls (Ctrol), in the presence and/or in absence of 4-PBA, apocynin and VAS2870. d mRNA levels of NOX2 and NOX4 in HUVECs incubated in plasma from patients with SLE with AN or Ctrol, in the presence and/or in absence of GW0742 and GSK0660. e Nitric oxide (NO) production estimated by the area under the curve (AUC) of the fluorescent signal of 4,5-diaminofluorescein (DAF-2) after stimulation with the calcium ionophore A23187 or insulin, in HUVECs incubated in plasma from patients with SLE with AN, or APS, or Ctrol, in the presence and/or in absence of 4-PBA, apocynin and VAS2870. Values are expressed as mean ± SEM (n = 5–6). * P < 0.05 and ** P < 0.01 vs Ctrol. # P < 0.05 and ## P < 0.01vs AN group without drugs. + P < 0.05 and ++ P < 0.01 vs GW0742 column

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