Augmenter of liver regeneration attenuates inflammation of renal ischemia/reperfusion injury through the NF-kappa B pathway in rats.

Abstract

The effects of augmenter of liver regeneration (ALR) on the acute kidney injury (AKI) rats were investigated by measuring the inflammatory response associated with transcription factor nuclear factory (NF-κB) pathway. The model of AKI rats was established by occluded the renal pedicles for 60 min and then released. After that, animals were treated with ALR (100 or 200 μg/kg). All rats were killed at different time points (24, 48, 72 h). Renal function and kidney histological changes were measured. The apoptosis of tubular cells was evaluated by TdT-mediated dUTP nick end labeling assay. Cytokines and chemokines were assessed by immunohistochemistry, enzyme-linked immunosorbent assay and real-time polymerase chain reaction (RT-PCR). The NF-κB p65 protein was analyzed by immunohistochemistry and RT-PCR, respectively. Ischemia reperfusion induced tubular cells necrosis and apoptosis, and ALR can significantly reduce this damages. The productions of MCP-1, IL-1β and IL-6 were lower in the group of ALR treatment, especially in the high-dose group. The inflammatory infiltrates were lower in the rats with administration of ALR. ALR mediated the level of cytokines and chemokines through inhibited the activation of NF-κB. ALR can improve renal function and inhibit the expression of inflammatory factors. This protects against renal ischemia reperfusion injury, which may be associated with preventing NF-κB activation in rats.