Short-term effect of atorvastatin on renal oxidative stress, inflammation, and fibrosis in a rat model of streptozotocin-induced diabetes

Diabetes mellitus (DM) contributes to the development and progression of nephropathy and kidney diseases. Statins are known to have anti-inflammatory and antifibrotic effects. We aimed to test the short-term effect of atorvastatin on renal biomarkers of oxidative damage, inflammation, and fibrosis in a rat model of streptozotocin-induced DM.

Wistar rats were divided into; control rats, rats treated with atorvastatin (Ator, oral 40 mg/kg for 6 weeks), DM rats (DM, one intraperitoneal 40 mg/kg streptozotocin), and atorvastatin-treated DM rats (DM + Ator). Renal oxidative stress markers, inflammatory and mitogenic factors were measured.

Streptozotocin induced an increase in serum glucose, blood urea nitrogen, and creatinine levels. A marked increase in kidney to body weight ratio was found in DM groups. Diabetes resulted in an elevation in inflammatory biomarkers of galectin-3 and endothelin-1. Hyperglycemia induced an increase in lipid peroxides and a decrease in the superoxide dismutase (SOD) antioxidant level in the DM group. A significant increase in the fibrotic factor platelet derived factor-BB (PDGF-BB) expression was documented in the DM group. Six weeks use of atorvastatin normalized kidney endothelin-1, galectin-3, and the PDGF-BB, and attenuated the increase in lipid peroxides and the reduction in SOD levels.

Our findings suggest that short-term use of atorvastatin may attenuate the substrates for diabetic nephropathy via partial decrease of renal markers of inflammation, oxidative stress, and fibrosis.