Chrysin protects against renal ischemia reperfusion induced tubular cell apoptosis and inflammation in mice.

Abstract

Renal ischemia reperfusion (IR) is a major cause of acute kidney injury with no effective treatment. Chrysin is an anti-inflammatory, anti-oxidant and anti-cancer agent. However, the effect of chrysin on renal IR injury remains unknown. In this study, sham operation, IR and IR+chrysin group mice were treated with or without renal IR injury. For renal IR, bilateral renal pedicles were clamped for 30 min and then released for 48 h of reperfusion. Blood and kidney samples were collected for analysis. Results demonstrated that chrysin pretreatment remarkably decreased the levels of serum creatinine and blood urea nitrogen and attenuated morphological abnormalities in renal IR injury. Consistently, tubular cell apoptosis and inflammation were more attenuated in the chrysin pretreatment group compared with the IR group. Chrysin pretreatment decreased the expression of Bax and cleaved caspase-3 and increased the expression of Bcl-2 in renal IR injury. Furthermore, chrysin administration decreased the mRNA and protein levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-6. Furthermore, the IκBα/nuclear factor-κB signaling pathway was more suppressed in the chrysin pretreatment group compared with the IR group. In conclusion, chrysin protects against tubular cell apoptosis and inflammation in renal IR injury.