Effect of Gracilaria fisheri sulfated galactan with increased sulfation on cell migration and expression of cell adhesion molecules in sodium oxalate-induced HK-2 cell injury.

Exposure to oxalate crystals causes cellular injury and dysfunction in the renal tubular epithelium. Sulfated galactan with increased sulfation (SGS) from the red seaweed Gracilaria fisheri exhibits anti-urolithiasis effects by inhibiting oxalate crystal formation and preventing sodium oxalate (NaOX)-induced death of renal tubular (HK-2) cells. However, the effects of SGS on wound healing and adhesion molecule expression in NaOX-induced HK-2 cell injury remain unexplored. The present study investigated the effects of SGS on wound healing and the regulation of adhesion molecule expression in NaOX-induced HK-2 cell damage. The findings showed that SGS promoted wound healing in HK-2 cells following a scratch injury under NaOX-induced conditions. NaOX exposure increased the expression of CD44 and vimentin while decreasing the expression of EpCAM, E-cadherin, occludin and ZO-1, as demonstrated by reverse transcription-quantitative PCR, western blotting and immunofluorescence analysis. Treatment with SGS restored these adhesion molecule expression levels to near normal. Scanning electron microscopy revealed that SGS also reversed NaOX-induced morphological changes in HK-2 cells. Additionally, SGS reduced the expression of Akt and p38 while upregulating PI3K and Erk1/2 in NaOX-treated HK-2 cells. These results suggested that SGS enhances wound healing and regulates the expression of adhesion molecules, possibly through the PI3K/Akt and MAPK (p38 and Erk1/2) signaling pathways, highlighting the potential of SGS as a promising therapeutic compound for preventing and treating NaOX-induced renal damage.