Regression of atherosclerosis by amlodipine via anti-inflammatory and anti-oxidative stress actions.

摘要: We examined whether amlodipine, an L-type calcium channel blocker (CCB), has inhibitory effect on oxidative stress and inflammatory response, thereby atherosclerosis, in apolipoprotein E-deficient (ApoEKO) mice. Adult male ApoEKO mice (6 weeks of age) were fed a high-cholesterol diet (HCD) for 8 or 10 with without oral administration amlodipine (3 mg/kg/day) only the last 2 HCD. After HCD feeding, atherosclerotic lesion formation, situ superoxide production nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity evaluated proximal aorta. The expressions NADPH subunits (p47(phox) rac-1), monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), vascular cell (VCAM-1) determined immunohistochemistry quantitative real-time reverse-transcription polymerase chain reaction. to mice, marked formation was observed In lesion, production, expression subunits, enhanced, MCP-1, ICAM-1, VCAM-1 increased. These changes suppressed that treated concomitant administration, no significant change blood pressure plasma cholesterol level. also treatment regressed lesions decrease inflammation. Inhibition area lipid aorta by correlated its actions stress, inflammation adhesive molecules. results suggest not inhibits but regresses these effects are at least partly due inhibition response.