Volume 3, Issue 4

 

Humoral markers of endothelial dysfunction and systemic inflammatory response in patients with acute myocardial infarction depending on genes polymorphism of ACE (I/D) and eNOS (894G>T)

 

Author: Larysa Sydorchuk, Yulia Ursuliak, Andriy Sydorchuk, Iryna Makoviychuk, Volodymir Trutiak, Igor Biryuk

Abstract: The dynamics of endothelial dysfunction (ED) humoral factors: a soluble form of vascular cell adhesion molecule 1 (sVCAM-1), total NO metabolites and systemic inflammatory response ­- C-reactive protein (CRP) in patients with acute myocardial infarction (MI) under the influence of treatment and depending on genes polymorphism – angiotensin converting enzyme (ACE, I/D) and endothelial nitric oxide synthase (eNOS, T894G) were evaluated. The presence of DD-genotype of ACE gene is associated with a significantly greater decrease of sVCAM-1 and CRP levels under the influence of treatment (better with thrombolytic therapy (TLT), p<0.05); in T- allele carriers of eNOS gene the level sVCAM-1 under TLT decreased by 30.7-31.2%. Content of NO metabolites decreased more in D-allele carriers of ACE gene as well as after combined treatment with TLT (39.1% and 35.2%) and did not depend on the allele state of eNOS gene.

Fig: Electrophoregramm of human DNA PCR products amplification of ACE I/D gene polymorphism. Note: L – DNA Ladder "GeneRuler 100 bp" (1000-100 bp); lines 1, 4 – homozygous II genotype; lines 2, 5 – heterozygous ID variant; lines 3, 6 – homozygous DD variant.

Fig: Electrophoregramm of human DNA PCR products amplification of ACE I/D gene polymorphism. Note: L – DNA Ladder "GeneRulerÔ 100 bp" (1000-100 bp); lines 1, 4 – homozygous II genotype; lines 2, 5 – heterozygous ID variant; lines 3, 6 – homozygous DD variant.

 

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