Effect of atorvastatin on the inflammatory response mediated by the nuclear factor κB65 in patients with acute myocardial infarction
10.3969/j.issn.1009-0754.2016.01.014
- VernacularTitle:阿托伐他汀对急性心肌梗死患者核因子 κB65介导炎症反应的作用
- Author:
Yu SUI
1
;
Chunyan WANG
Author Information
1. 龙口市人民医院
- Keywords:
Acute myocardial infarction;
Nuclear factor-κB;
Inflammatory cytokine;
Atorvastatin
- From:
Journal of Navy Medicine
2016;37(1):40-42
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the inflammatory response mediated by the nuclear factor κB65(NF-κBp65)in patients with acute myocardial infarction and to evaluate the effect of atorvastatin on the inflammatory response .Methods Seventy-eight patients with acute myocardial infarction (AMI) were randomly divided into group A and group B , which were respectively given 20 mg and 40 mg of atorvastatin before sleep , in addition to routine treatment .Another 30 healthy adults were chosen as the control group .The levels of NF-κBp65 in the AMI patients were determined and changes in NF-κBp65-mediated inflammatory factors were analyzed statistically .Results The levels of NF-κBp65, MCP-1, IL-1 and IL-6 in AMI patients were all higher than those of the healthy population , with statistical sig-nificance (P<0.05).Following treatment, the levels of NF-κBp65, MCP-1, IL -1 and IL-6 in the AMI patients were all significantly lower than those before treatment (P<0.05), also with statistical significance (P<0.05).ALT and CK levels were significantly higher than those before treatment , with statistical significance (P<0.05).Following treatment, the levels of NF-κBp65, MCP-1, IL-1 and IL-6 in the patients of group B were significantly lower than those in the patients of group A , also with statistical significance (P<0.05). Conclusion Acute myocardial infarction was the advanced stage of atherosclerosis and NF -κB-mediated inflammatory response was close-ly associated with the onset of the disorder .Atorvastatin might decrease the levels of NF-κBp65, MCP-1, IL-1 and IL-6 by inhibiting the expression of NF-κB in patients with acute myocardial infarction and this inhibitive effect seemed to be dose dependent .
