Role of atorvastatin in improving the inflammation-induced adipokine imbalance in mice with acute myocardial infarction

Abstract

To investigate the effect of acute myocardial infarction (AMI)-activated inflammation on adipokine imbalance and the therapeutic effects of statin. Methods: A total of 32 C57BL/6 mice were divided into 4 groups: a sham group, an AMI group, a low-dose atorvastatin [2 mg/(kg.d)] group and a high-dose atorvastatin [20 mg/(kg.d)] group. AMI models were established by surgical coronary artery ligation. Plasma levels of high sensitive C reaction protein (hs-CRP), adiponectin and resistin were measured. Adiponectin and resistin expressions were determined. In addition, mouse 3T3-L1 preadipocytes in vitro were differentiated and they were stimulated by oxidized low density lipoprotein (ox-LDL). The protein expressions of adiponectin and resistin in adipocytes were detected. The effects of atorvastatin on ox-LDL-induced adipokine imbalance in adipocytes were identified. Results: The plasma levels of hs-CRP and resistin in AMI mice were significantly increased, whereas the plasma levels of adiponectin were remarkably decreased. However, atorvastatin treatment blocked the changes in the plasma levels of hs-CRP, resistin and adiponectin in AMI mice in a dose-dependent manner. Consistent findings regarding the adipose expressions of the two adipokines were obtained. The plasma levels of hs-CRP were positively correlated with resistin but negatively with adiponectin. In vitro study, ox-LDL increased resistin protein and adiponectin expressions in adipocytes, which were dose-dependently reversed by atorvastatin. Conclusion: Inflammation activation in AMI mice leads to adipokine imbalance. Atorvastatin ameliorates the AMI-induced adipokine imbalance via anti-inflammation.