KMID : 0191120140290000139
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Journal of Korean Medical Science 2014 Volume.29 No. 0 p.139 ~ p.145
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Cobalt Chloride Attenuates Oxidative Stress and Inflammation through NF-¥êB Inhibition in Human Renal Proximal Tubular Epithelial Cells
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Oh Se-Won
Lee Yun-Mi Kim Se-Joong Chin Ho-Jun Chae Dong-Wan Na Ki-Young
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Abstract
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We evaluated the effect of cobalt chloride (CoCl2) on TNF-¥á and IFN-¥ã-induced-inflammation and reactive oxygen species (ROS) in renal tubular epithelial cells (HK-2 cells). We treated HK-2 cells with CoCl2 before the administration of TNF-¥á/IFN-¥ã. To regulate hemeoxygenase-1 (HO-1) expression, the cells were treated CoCl2 or HO-1 siRNA. CoCl2 reduced the generation of ROS induced by TNF-¥á/IFN-¥ã. TNF-¥á/IFN-¥ã-treated-cells showed an increase in the nuclear translocation of phosphorylated NF-¥êBp65 protein, the DNA-binding activity of NF-¥êBp50 and NF-¥êB transcriptional activity and a decrease in I¥êB¥á protein expression. These changes were restored by CoCl2. We noted an intense increase in monocyte chemoattractant protein-1 (MCP-1) and regulated on activation normal T cell expressed and secreted (RANTES) production in TNF-¥á/IFN-¥ã-treated cells. We demonstrated that this effect was mediated through NF-¥êB signaling because an NF-¥êB inhibitor significantly reduced MCP-1 and RANTES production. CoCl2 effectively reduced MCP-1 and RANTES production. The expression of HO-1 was increased by CoCl2 and decreased by HO-1 siRNA. However, knockdown of HO-1 by RNA interference did not affect MCP-1 or RANTES production. We suggest that CoCl2 has a protective effect on TNF-¥á/IFN-¥ã-induced inflammation through the inhibition of NF-¥êB and ROS in HK-2 cells. However, CoCl2 appears to act in an HO-1-independent manner.
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KEYWORD
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Cobalt Chloride, Hemeoxygenase-1, Inflammation, Nuclear Factor-kappa B, Renal Tubular Epithelial Cells
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