Abstract
BackgroundRecent studies in animal models have shown that statins can protect against renal failure independent of their lipid-lowering actions, and there is also an association between statin use and improved renal function after suprarenal aortic clamping. We investigated the hypothesis that post-ischemic acute renal failure could be ameliorated with atorvastatin (ATO) treatment and the possible molecular mechanisms in a model of ischemia–reperfusion (IR) in rats.MethodsTwenty-four male Sprague–Dawley rats were divided into three groups: sham, IR, and IR + ATO. ATO was given by a single intraperitoneal injection (10 mg/kg) 30 min before reperfusion in the IR + ATO group. The IR group and sham group received saline vehicle via the intraperitoneal route.ResultsAfter 24 h of IR, serum creatinine levels were increased in the IR group compared with the sham group (p < 0.001). ATO treatment reduced the elevation of serum creatinine level by 18% (p < 0.05) and significantly increased the creatinine clearance rate (p < 0.001). Concentrations of advanced oxidation protein products and malondialdehyde were reduced in the ATO group, approaching levels observed in sham-group rats. ATO treatment alleviated pathological changes in renal tubular cells. Protein and mRNA levels of intercellular adhesion molecule-1 and monocyte chemotactic protein-1 were reduced significantly.ConclusionsThese data suggest that direct protection of injured kidneys by ATO was possible even though the drug was injected 30 min before reperfusion, and that ATO may reduce IR injury by anti-inflammatory effects and by reducing oxidation stress.
Highlights
Recent studies in animal models have shown that statins can protect against renal failure independent of their lipid-lowering actions, and there is an association between statin use and improved renal function after suprarenal aortic clamping
Recent studies have shown that reactive oxygen species (ROS), inflammatory mediators such as intracellular adhesion molecule (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) [7,8] as well as infiltration of inflammatory cells are implicated in renal ischemia–reperfusion injury [2]
These findings suggest an association between statin use and preserved renal function in acute renal failure (ARF) scenarios such as suprarenal aortic clamping, kidney transplantation, and critically ill patients in the intensive care unit [12,13], they carry little significance in patients with unpredictable ARF caused by hemorrhage, severe injury, or shock
Summary
Recent studies in animal models have shown that statins can protect against renal failure independent of their lipid-lowering actions, and there is an association between statin use and improved renal function after suprarenal aortic clamping. The effects of statins in ischemia–reperfusion models of renal protection have been related to their antiinflammatory, antioxidant, and vascular actions [9,10,11] These findings suggest an association between statin use and preserved renal function in ARF scenarios such as suprarenal aortic clamping, kidney transplantation, and critically ill patients in the intensive care unit [12,13], they carry little significance in patients with unpredictable ARF caused by hemorrhage, severe injury, or shock. In these studies, statin intervention has been several days before ischemia–reperfusion injury. The present study was undertaken to examine the effects and mechanisms of atorvastatin (ATO) after renal ischemia–reperfusion injury with focuses on tubular damage, necrosis, inflammation and oxidant stress in rats
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