Inflammation Activation Contributes to Adipokine Imbalance in Patients with Acute Coronary Syndrome

PLoS One. 2016 Mar 17;11(3):e0151916. doi: 10.1371/journal.pone.0151916. eCollection 2016.

Abstract

Inflammation can be activated as a defensive response by the attack of acute coronary syndrome (ACS) for ischemic tissue injury. The aim of the present study was to investigate the impact of ACS-activated inflammation on adipokine imbalance and the effects of statins on the crosstalk between inflammation and adipokine imbalance during ACS. In this study, 586 subjects were categorized into: (1) control group; (2) SA (stable angina) group; and (3) ACS group. Circulating levels of hs-CRP, adiponectin and resistin were measured by ELISA. Furthermore, forty C57BL/6 mice were randomized into: sham, AMI, low-statin (atorvastatin, 2 mg/kg/day) and high-statin (atorvastatin, 20 mg/kg/day) group. After 3 weeks, AMI models were established by surgical coronary artery ligation. Circulating levels and adipose expressions of adiponectin and resistin were assessed in animals. Besides, we investigate the effects of atorvastatin on ox-LDL-induced adipokine imbalance in vitro. As a result, we found that ACS patients had higher hs-CRP and resistin levels and lower adiponectin levels. Our correlation analysis demonstrated hs-CRP concentrations were positively correlated with resistin but negatively with adiponectin levels in humans. Our animal findings indicated higher circulating hs-CRP and resistin levels and lower adiponectin levels in AMI mice. Atorvastatin pre-treatment dose-dependently decreased hs-CRP and resistin levels but increased adiponectin levels in mice. The consistent findings were observed about the adipose expressions of resistin and adiponectin in mice. In study in vitro, ox-LDL increased cellular resistin expressions and otherwise for adiponectin expressions, which dose-dependently reversed by the addition of atorvastatin. Therefore, our study indicates that the ACS attack activates inflammation leading to adipokine imbalance that can be ameliorated by anti-inflammation of atorvastatin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Coronary Syndrome / drug therapy
  • Acute Coronary Syndrome / etiology
  • Acute Coronary Syndrome / physiopathology*
  • Adipokines / physiology*
  • Adiponectin / blood
  • Animals
  • Atorvastatin / therapeutic use
  • Blotting, Western
  • C-Reactive Protein / analysis
  • Female
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use
  • Inflammation / complications
  • Inflammation / drug therapy
  • Inflammation / physiopathology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Middle Aged
  • Myocardial Infarction / etiology
  • Myocardial Infarction / physiopathology
  • Resistin / blood

Substances

  • Adipokines
  • Adiponectin
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Resistin
  • C-Reactive Protein
  • Atorvastatin

Grants and funding

This work was funded by the National Natural Science Foundation of China (http://www.nsfc.gov.cn/) under Grant No. 81000121.