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Background: To evaluate the effects of contrast agents containing increasing concentrations of iodine on the renal oxygenation level determined by blood oxygenation level dependent (BOLD) magnetic resonance imaging (MRI) in a rabbit model of diabetic nephropathy. Methods: BOLD-MRI was performed using saline or iodinated (I) contrast agents (200, 240, 300, 350 and 400 mg I/mL) at 1, 24, 48, and 72 h after experimentally inducing type 2 diabetic nephropathy in rabbits. Differences in renal oxygenation levels between type 1 and type 2 diabetic nephropathy were also assessed by BOLD-MRI after injecting 400 mg I/mL of contrast agent. Results: Contrast agents increased the R2* values of the renal cortex, outer medulla, and inner medulla to the maximum levels at 24 h. The R2* values then decreased to their lowest levels at 72 h. The R2* was highest following injection of 400 mg I/mL, especially in the outer medulla. The R2* values were not significantly different between types 1 and 2 diabetic nephropathy. Conclusions: Iodinated contrast agents had the greatest influence on renal outer medulla oxygenation level at 24 h in type 2 diabetic nephropathy, with the greatest effects observed at the 400 mg I/mL dose level. There were no differences in BOLD-MRI values between type 1 and type 2 diabetic nephropathy after administering the contrast agent at 400 mg I/mL. [ABSTRACT FROM AUTHOR]

We demonstrate that activation of nuclear factor κB (NF-κB) in neurons is neuroprotective in response to kainic acid (KA)-induced excitotoxicity. Combination of Western blotting, immunocytochemistry, and electrophoresis mobility shift assay showed that KA exposure induced a fast but transient nuclear translocation of the NF-κB p65 subunit and increased DNA-binding activity of NF-κB in primary cultured cortical neurons. The transient NF-κB activity was associated with upregulation of antiapoptotic Bcl-xL and XIAP gene products revealed by real-time PCR. Knockdown of p65 decreased neuronal viability and antiapoptotic gene expression. In addition, we showed that KA-stimulated DNA-binding activity of NF-κB was associated with reactive oxygen species and calcium signals, using AMPA/KA receptor antagonist, calcium chelator, and antioxidant. These results suggest that the fast and transient activation of NF-κB initiated by calcium signals is one of the important proximal events in response to KA-induced excitotoxicity, which has neuroprotective effect against KA-induced apoptosis. [ABSTRACT FROM AUTHOR]