In agreement with previous reports, our present results indicate that high glucose may be involved in the pathogenesis of DN via manifesting upregulation of phosphorylation of IκBα, which results in IκBα degradation and activation of NF-κB. Our experimental results also showed that the release of MCP-1 and IL-6 from GMCs was significantly upregulated by high glucose in a dose-dependent and time-dependent manner, suggesting that high glucose induces a renal inflammatory state. This evidence concerns the gene CCL2 and liver dysplastic nodule.