Prevention and possible mechanism of a purified Laminaria japonica polysaccharide on adriamycin-induced acute kidney injury in mice.

The present work aims to investigate the effects and underlying mechanism of a homogeneous Laminaria japonica polysaccharide (LJP61A) on acute kidney injury (AKI) in mice. According to the results of biochemical and pathological analysis, we concluded that LJP61A could protect kidney from the damage of adriamycin in AKI mice. Compared to the model group, the mRNA level of cytokines (TNF-α, IL-1β and MCP-1) and protein level of mesenchymal markers demsin were decrease by the treatment of LJP61A while the protein levels of podocyte structure markers (Nephrin and WT-1) were increased. Moreover, the adriamycin-induced enhancement of phosphor-p65, phosphor-p38, phosphor-ERK1/2 and phosphor-JNK in the kidney of AKI mice were significantly suppressed by LJP61A. Similar variation was observed in the mRNA and protein levels of TGF-β1 and Smad3. These results suggested that LJP61A prevented acute kidney injury possibly via regulating TGF-β1-mediated Smad3, MAPKs and NF-κB signaling pathways.