Atorvastatin downregulates monocyte CD36 expression,nuclear NFκB and TNFα levels in type 2 diabetes

Aim: type 2 diabetes increases the risk for cardiovascular disease,and 3-hydroxy-3-methylglutaryl coenzyme a (hmg-coa) reductase inhibitors (statins) reduce cardiovascular events in these patients. the benefits of statin therapy cannot be explained only by the lipid-lowering effect. the aim of this study was to test the effect of atorvastatin therapy on cd36 scavenger receptor expression,nuclear factor-kappab (nfκb) levels and markers of inflammation (c-reactive protein,crp,tumor necrosis factor-α,tnf-α) in circulating monocytes from diabetic patients. methods: twenty-two type 2 diabetic patients were treated for 8 weeks with atorvastatin (20 mg/day). at baseline and after treatment a blood sample was collected for measurement of glucose,lipid profile (total cholesterol,hdl,ldl cholesterol,triglycerides),glycated hemoglobin (hba1c),crp and for isolation of monocytes. results: atorvastatin decreased total (p<0.0001) and ldl (p<0.01),and incresased hdl cholesterol (p<0.02). cd36 surface protein expression (anti-cd36 fluorescein isothiocyanate-fitc) was reduced in circulating monocytes after atorvastatin therapy (p<0.02) while immunoblot analysis showed reduced nuclear and increased cytoplasm nfκb levels (p<0.05). finally,tnfα production in lipopolysaccharide-activated monocytes from patients treated with atorvastatin was reduced (p<0.05). conclusion: these results suggest that atorvastatin therapy,beside lowering serum cholesterol levels,could exert anti-atherogenic and anti-inflammatory effects in type 2 diabetic patients.