Abstract
Ischemia/reperfusion may induce inflammation and cell death through the nuclear factor (NF)‑κB signaling pathway. As a negative regulator of NF‑κB, zinc finger A20 exhibits anti-apoptotic and anti‑inflammatory effects in vitro. The present study was designed to upregulate A20 expression using an A20 transfection approach to investigate the in vivo protective effects of the A20 gene on renal ischemia reperfusion injury. The A20 gene was cloned into a pcDNA3.1 vector to construct the expression plasmid pcDNA3.1‑A20. The plasmid was wrapped with a liposome and injected intravenously into rats 48 h prior to establishing the models of renal ischemia reperfusion injury. Saline and the empty plasmid pcDNA3.1 were used as controls. Following 24 h post‑operation, A20 expression was determined using reverse transcription‑quantitative polymerase chain reaction and western blotting. The renal function and structure were assessed by analyzing the concentrations of serum creatinine (Scr), blood urea nitrogen (BUN) and histological features. Renal tissues were additionally examined for renal tubular cell apoptosis and NF‑κB activity. The results demonstrated that in vivo transfection of pcDNA3.1‑A20 induced renal A20 expression in rats. A20 overexpression in vivo significantly reduced renal injury as demonstrated by the improved levels of Scr and BUN and the reduction in histological damage. These improvements were accompanied by a suppression of renal proximal tubular epithelial cell apoptosis and an inhibition of NF‑κB activity. These results indicated that transfection of the A20 gene upregulates the expression of A20 in vivo and protects the kidneys from ischemia reperfusion injury via inhibition of the NF‑κB signal transduction pathway.