Objective To investigate the regulatory mechanism of PI3K/AKT/NF-κB signaling pathway in uric acid-induced renal cell injury by observing the change of expression level in a rat model of uric acid nephropathy.

Methods Thirty-six male SD rats were randomly divided into experimental group (n=18) and control group (n=18). The rats in the experimental group were given adenine and ethambutol by gavage to establish the model of hyperuricemia nephropathy. The control group was given the same amount of normal saline gavage. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the gene expression levels of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) and nuclear factor κB (NF-κB); western blot method was used to detect the protein expression levels of PI3K, AKT and NF-κB in each group; Enzyme Linked Immunosorbent Assay (ELISA) method was used to detect the expression level of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), pro-interleukin-1β (Pro-IL-1β), interleukin-1β (IL-1β) and transforming growth factor-β1 (TGF-β1).

Results The mRNA expression levels of PI3K, AKT and NF-κB in the experimental group were significantly higher than those in the control group (P < 0.05 or P < 0.01). The expression of PI3K, AKT and NF-κB proteins in the experimental group were significantly higher than those in the control group (P < 0.05 or P < 0.01). The levels of TNF-α, McP-1, IL-6, Pro-IL-1β and IL-1β in the experimental group were significantly higher than those in the control group (P < 0.05 or P < 0.01).

Conclusion High uric acid may induce renal interstitial inflammation and renal interstitial fibrosis by activating PI3K/AKT/NF-κB signaling pathway, and may be involved in the occurrence and development of uric acid nephropathy.