SDF-1α upregulation by atorvastatin in rats with acute myocardial infarction via nitric oxide production confers anti-inflammatory and anti-apoptotic effects

Background: the effects of atorvastatin on sdf-1α expression under acute myocardial infarction (ami) are still unclear. therefore,our present study is to investigate the roles and mechanisms of atorvastatin treatment on sdf-1α expression in rats with ami. methods. male sprague-dawley rats were underwent permanent coronary artery ligation and randomly assigned into four groups as follow: blank control (b),atorvastatin (a),atorvastatin plus l-name (a+l-name),and atorvastatin plus amd3100 (a+amd3100). rats underwent similar procedure but without ligation were used as group sham operated (s). atorvastatin (10mg/kg/d body weight) was administrated by gavage to rats in three atorvastatin treated groups,and l-name (40mg/kg/d body weight) or amd3100 (5mg/kg/d body weight) was given to group a+l-name or a+amd3100,respectively. results: comparing with group b,no production,sdf-1α and cxcr4 expression were significantly up-regulated in three atorvastatin treated groups at the seventh day. however,the increments of sdf-1α and cxcr4 expression in group a+l-name were reduced when no production was inhibited by l-name. anti-inflammatory and anti-apoptotic effects of atorvastatin were offset either by decrease of sdf-1α and cxcr4 expression (by l-name) or blockage of sdf-1α coupling with cxcr4 (by amd3100). expression of stat3,a cardioprotective factor mediating sdf-1α/cxcr4 axis induced cardiac protection,was up-regulated most significantly in group a. the effects of atorvastatin therapy on cardiac function were also abrogated either when sdf-1α and cxcr4 expression was diminished or the coupling of sdf-1α with cxcr4 was blocked. conclusion: sdf-1α upregulation by atorvastatin in rats with ami was,at least partially,via the enos/no dependent pathway,and sdf-1α upregulation and sdf-1α coupling with cxcr4 conferred anti-inflammatory and anti-apoptotic effects under ami setting which we speculated that ultimately contributed to cardiac function improvement. © 2012 qiu et al.; licensee biomed central ltd.