Effects of kallistatin on oxidative stress and inflammation on renal ischemia-reperfusion injury in mice.

Abstract

Kallistatin (KS) is a serine proteinase. The result of KS on 'Renal Ischemia- Reperfusion Injury' (IRI) has not clearly been researched. In this study, investigative research has been conducted to draw results on the administration of human KS on kidney response conducted within a mouse model of IRI. BALB/c mice were used and given 30 min ischemia that was injected into the kidney which was followed with 24 h reperfusion. The human KS gene contained within an adenoviral vector was injected intravenously 30 min before reperfusion and 12h after reperfusion. Analyses illustrated what impact KS had on renal IRI in realtion to tubular necrosis, apoptotic cell death, inflammatory cytokines, renal function, and inflammatory cell infiltration. KS gene transfer significantly had a positive impact on renal function (reduced blood urea-nitrogen: 73.5±13.6 vs. 195.4±14.6 mg/dL at day three, p < 0.05 and the serum creatinine levels: 0.23±0.02 vs. 0.71±0.14 mg/dL at day three, p < 0.05), reduced tubular necrosis and apoptosis of IRI kidneys. The permeation of cells that were inflamed and the manufacturing of pro-inflammatory cytokines (RANTES-is regulated through been activated with normal T-cell which are expressed and secreted, tumour necrosis interleukin-1β factor-α, and interferon-γ) resulted in significantly suppressing KS in mice with IRI. The efficacy to scavenge superoxide in tubule cells was also demonstrated by high-performance liquid chromatography. Our study suggests a novel role of KS in renal protection after 'Renal Ischemia-Reperfusion Injury' blocking of oxidative stress and renal inflammation.