Therefore, the effect of CaD to decrease CD14 and TLR4 expression could offer one mechanism to explain why CaD inhibits NF-κB and suppresses the release of downstream NF-κB activation products—TNFα, IL-1β, IL-6, and MCP-1 in animal models of sepsis and diabetic nephropathy and retinopathy [11,13,14,32]. Here, CCL2 is linked to diabetic kidney disease.