The Role Of Autophagy In Soluble Uric Acid-induced Inflammatory Response Of Renal Tubular Epithelial Cells

Objective: To investigate the role of autophagy in the inflammation induced by soluble uric acid in renal tubular epithelial cells(HK-2 cells).Methods: After HK-2 cells being stimulated by soluble uric acid solution,the changes of autophagosomes volume were observed by transmission electron microscopy.Western blotting was used to detect monocyte chemoattractant protein-1(MCP-1),autophagic microtubule-associated light chain protein 3(LC3-II)and autophagy-related regulatory protein Beclin1 expression.Next,HK-2 cells were co-stimulated with soluble uric acid and rapamycin(RAP)or chloroquine(CQ).Transmission electron microscopy was used to observe autophagosomes and western blotting was used to detect the expression of MCP-1,LC3-II and Beclin1.Furthermore,HK-2 cells were co-stimulated with Akt inhibitor Perifosine and soluble uric acid solution,and the expression of p-Akt and MCP-1 was detected by western blotting.Results: The expression of MCP-1,LC3-II,and Beclin1 in HK-2 cells was up-regulated by soluble uric acid,and the number of autophagy increased as observed by the transmission electron microscope(TEM).When the HK-2 cellswere stimulated by rapamycin and soluble uric acid,the expression of autophagy was further enhanced and the expression of MCP-1 was weakened as compared with the single use of soluble uric acid.Meanwhile,chloroquine inhibited the autophagy of soluble uric acid and increased the expression of MCP-1.The expression of MCP-1 decreased after co-stimulation of Akt blocker Perifosine and uric acid.Conclusion: Soluble uric acid can induce tubular epithelial cell inflammation and promote autophagy in HK-2 cells.Autophagy is involved in the regulation of soluble uric acid-induced inflammation in renal tubular epithelial cells.