Kaempferol improves acute kidney injury via inhibition of macrophage infiltration in septic mice

Sepsis contributes to life-threatening circulatory and organ dysfunction by dysregulating the host response to infection in critically ill patients. Treatment in an Intensive Care Unit (ICU) can improve the survival of patients who suffer from severe sepsis, but sepsis-associated acute kidney injury (SAKI) is still one of the main causes of death. The existing treatment is mainly focused on controlling microorganism induced infections by using drugs, such as ulinastatin and glucocorticoid. Also, it is well documented that kaempferol, a flavonoid derived from plant sources, improves septic mouse survival via anti-inflammatory response. However, the mechanism of anti-inflammatory response mediated by this flavonoid compound was little known. This study aims to demonstrate the mechanisms of inflammatory response regulated by kaempferol treatment during sepsis. We perform cecal ligation and puncture (CLP) injury as a sepsis mouse model and evaluate organ injury in sepsis. The molecular (qRT-PCR and Western Blot) and cellular profiling (IHC staining and Flow Cytometry) of the immune responses illustrates that kaempferol decreases the expression of adhesion molecular genes (ICAM-1 and VCAM-1) and monocyte chemoattractant protein-1 (MCP-1), thereby inhibiting F4/80+ macrophages infiltration in CLP-induced acute kidney injury. Our data suggested that kaempferol alleviates acute kidney injury via regulating F4/80+ macrophages infiltration in CLP-induced acute kidney injury.