José Marcos Girardi
Rogério Estevan Farias
Ana Paula Ferreira
Nádia Rezende Barbosa RaposoI
OBJECTIVE
The aim of the present study was to assess the effects of rosuvastatin on renal injury and inflammation in a model of nitric oxide deficiency.
METHODS
Male Wistar rats were randomly divided into four groups (n = 10/group) and treated for 28 days with saline (CTRL); 30 mg/kg/day L-NAME (L-name); L-NAME and 20 mg/kg/day rosuvastatin (L-name+ROS-20); or L-NAME and 2 mg/kg/day rosuvastatin (L-name+ROS-2). Systolic blood pressure was measured by plethysmography in the central artery of the tail. The serum total cholesterol, triglycerides, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, creatinine, nitric oxide, interleukin-6, and tumor necrosis factor alpha levels were analyzed. Urine samples were taken to measure the albumin5urinary creatinine ratio. Kidneys were sectioned and stained with hematoxylin/eosin and Masson’s trichrome. Immunohistochemical analysis of the renal tissue was performed to detect macrophage infiltration of the glomeruli.
RESULTS
The systolic blood pressure was elevated in the L-name but not the L-name+rosuvastatin-20 and L-name+rosuvastatin-2 groups. The L-name group had a significantly reduced nitric oxide level and an increased interleukin-6 and tumor necrosis factor alpha level, albumin5urinary creatinine ratio and number of macrophages in the renal glomeruli. Rosuvastatin increased the nitric oxide level in the L-name+rosuvastatin-2 group and reduced the interleukin-6 and tumor necrosis factor alpha levels, glomerular macrophage number and albumin5urinary creatinine ratio in the L-name+rosuvastatin-20 and L-name+rosuvastatin-2 groups.
CONCLUSION
Rosuvastatin treatment reduced glomerular damage due to improvement in the inflammatory pattern independent of the systolic blood pressure and serum lipid level. These effects may lead to improvements in the treatment of kidney disease.
KEYWORDS: L-NAME; Hypertension; HMG-CoA reductase inhibitors; Kidney; Interleukins.
