-13T/C Polymorphism Of Saa 5'-Flanking Region In Ischemic Cerebrovascular Diseases

Background and objectiveIschemic cerebrovascular diseases induced by atherosclerosis are serious hazard diseases affecting human health. As one of the pathogenesis of atherosclerosis, inflammation and its genetic predisposition play an important role in the development of ischemic cerebrovascular diseases. Serum Amyloid A Protein (SAA) is an acute inflammatory markers. This paper is to detect the association between -13T/C single-nucleotide polymorphisms (SNPs) at the 5'-flanking region of SAA and ischemic cerebrovascular diseases and to investigate the mechanisms by which SAA polymorphisms are involved by examining serum concentrations of SAA.MethodsUsed enzyme-linked immunosorbent assay (ELISA) to detect the serum levels of SAA and Matrix Metalloproteinases-9 (MMP-9) of 193 cases with ischemic cerebrovascular diseases (including cerebral infarction and transient ischemic attack) and 120 healthy. Used radioimmunoassay detected the serum levels of C-reactive protein (CRP). Analyzed single-nucleotide polymorphism -13T/C at the 5'-flanking region (rs:11024595) of DNA samples came from 291 cases with ischemic cerebrovascular diseases and 226 healthy by polymerase chain reaction (PCR) and gel electrophoresis imaging techniques.ResultsSerum levels of SAA are higher in ischemic cerebrovascular diseases subjects than in healthy subjects (t= 8.571,9.905,8.135; P<0.01). There is a positive correlation between SAA and CRP and MMP-9 in ischemic cerebrovascular diseases (r=0.494,0.454,P<0.01). Both genotypes and allele frequencies of-13T/C at the 5'-flanking region have no significant differences in the two groups (P> 0.05). The polymorphisms of -13T/C has no association with ischemic cerebrovascular diseases.ConclusionsThe data suggest that as an inflammatory marker of atherosclerosis, SAA paricpates in the occurrence and development of ischemic cerebrovascular disease, but if can SAA be an independent risk factor of ischemic cerebrovascular disease or not should be confirmed by a large number of clinical and experimental studies. Its -13T/C polymorphism may be no association with ischemic cerebrovascular diseases, but other sites'has yet to be verified.