Background: 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.
Materials and Methods: 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.
Results: 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
Conclusion: Our study suggests a novel role of KS in renal protection after ‘Renal Ischemia-Reperfusion Injury’ blocking
of oxidative stress and renal inflammation.