Manuscript accepted on :04-12-2019
Published online on: 24-12-2019
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585Shakir F. T. Alaaraji
Department of Chemistry, College of Education for Pure Sciences, University of Anbar, Rammadi, Iraq
Corresponding Author E-mail: esp.shaker.faris@uoanbar.edu.iq
DOI : https://dx.doi.org/10.13005/bpj/1846
Abstract
Acute Myocardial infarction (AMI) is one of the important reasons of loss of life and bodily incapacity global prompt via cardiovascular diseases (CVD). AMI stimulates the innate immune system that is required to employee leukocytes to remove necrotic cells and recruit myocardial healing. To evaluate serum concentrations of Monocyte Chemoattractant Protein-1 (MCP-1), Autotaxin (ATX), Azurocidin-1 (AZU-1), Apolipoprotein C-III (APOC3) and Elastase-2 (ELA-2) in male Iraqi AMI patients and healthy controls (HCs), and explain the association of MCP-1with ATX, AZU-1, APOC3 and ELA-2 in male Iraqi AMI patients, also explore the best parameter which can use to differentiate between AMI patients. This case-control study included 84 men aged 40–68 years. Waist circumference (WC), hip circumference (HC), thoracic circumference (TC), neck circumference (NC), height, weight, age, and further covariates were obtained via an inquiry form. They were separated into two equivalent groups: the patients group and the healthy group, serum concentrations of MCP-1, ATX, AZU-1, APOC3 and ELA-2 were estimated via ELISA. Serum of MCP-1, ATX, AZU-1, APOC3 and ELA-2 concentrations were importantly greater in patients with AMI than in HCs (p< 0.001). MCP-1 concentrations were importantly linked with ATX, AZU-1, APOC3 and ELA-2 in AMI cases (p< 0.001). The greater value of MPC-1 association was with ELA-2 (r=0.592). MCP-1 exhibited the maximum value for área under curve (AUC=1) in comparison to other studied biomarkers. The present data explained the role of MCP-1, ATX, AZU-1, APOC3 and ELA-2 in AMI disease; we found they have central functions in this disease, mainly obese patients. Attention must be taken to avoid confusion among risk markers and risk factors. Great serum concentrations of MCP-1 offered important correlations between risk markers and risk factors of AMI disease.
Keywords
MCP-1; Autotaxin; Apolipoprotein C-III; Acute Myocardial Infraction
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| Copy the following to cite this article: Alaaraji S. F. T. Is there a Correlation between Monocyte Chemoattractant Protein-1 with Autotaxin, Azurocidin-1, Apolipoprotein C-III and Elastase-2 in Male Iraqi Acute Myocardial Infraction Patients? Biomed Pharmacol J 2019;12(4). |
| Copy the following to cite this URL: Alaaraji S. F. T. Is there a Correlation between Monocyte Chemoattractant Protein-1 with Autotaxin, Azurocidin-1, Apolipoprotein C-III and Elastase-2 in Male Iraqi Acute Myocardial Infraction Patients? Biomed Pharmacol J 2019;12(4). Biomed Pharmacol J 2019;12(4). Available from: https://bit.ly/2ESoUwk |
Introduction
Acute Myocardial infarction (AMI), a medical problem of coronary atherosclerosis, mainly grows from the separation of an atherosclerotic plate with formation of thrombus and coronary vessel blocking [1], this leads to a severe decrease in the supply of blood to the heart muscle [2]. Risk factors such as hyperlipidemia hypertension, smoking, obesity and diabetes mellitus were stated to be related with augmented AMI risk [3]; nonetheless, the fundamental mechanisms which lead to AMI not yet determined. It’s, a complex multifaceted illness, is happened via together genetic tendency and environmental causes [4].
Previous paper indicated that abnormal immune reply grows through AMI which is harmful and involves to death of cell after the abuses [5]. AMI is described via of adhesion molecules, proinflammatory cytokines expression, and essentially, chemokines that help the leukocytes infiltration into area of infarct, expression of harmful mediators and complement system activation [6].
Chemokines are inflammatory cytokines subset that contribute in the leukocytes employment to locations of irritation and are assembled into subfamilies: CXC and CC chemokines [7]. MCP-1 is one of the well-studied CC chemokine; it’s shown an important relationship with danger elements for CVD like hypertension, renal insufficiency, diabetes and age, [8]. MCP-1 may activate the atherosclerosis (AS) progress and development of via monocyte permeation activating and fat-laden foam cells growth [9]. The most important, one research showed that MCP-1 could exert a central function in AMI damage and inverse remodeling by various possible mechanisms [10].
Autotaxin (ATX) which is overexpressed in valves of mineralized aortic is a lysophospholipase-C that hydrolyses ox-Phos into lysophosphatitic acid (LPA) [11]. LPA is a highly bioactive complex which activates several inflammatory manners involving fibrosis. The most important, one research showed that LPA and ATX are included in the AS pathobiology [12]. LPA encourages hypertrophy of cardiomyocyte through encouraging the initiation signals of Rho‐intermediated [13]. Nonetheless, whether LPA/ATX signalling is included in the development of obesity‐linked AMI is still unidentified, previous paper had established that LPA, manufactured via ATX, stimulates irritation and controls monocytosis [14].
Azurocidin (AZU) an antimicrobial protein involved in the serprocidin subclass of chymotrypsin-like proteases [15, 16]. AZU is existed in secretory vesicles of the neutrophils and granules of azurophilic [17]. Adhesion of Neutrophilic to the endothelium through irritation stimulates the excrete of basal AZU from secretory vesicles and granules of azurophilic [16, 17]. AZU, as a protein with multifunctional, is an essential compound in the reply of host through contagion [15]. The physiological roles of AZU involve monocyte recruitment stimulation to the site of irritation, increase phagocytosis of macrophage, and antimicrobial action [15–17]. It’s similarly rises efflux of macromolecular via cellular barriers breaking and permeability of endothelial [18].
Apolipoprotein C-III (APOC3) was recognized from about six decades as a controller of circulation triglyceride rich lipoproteins (TRLs) [19]. Furthermore to possess great ability to prevent mediated lipolysis of LPL; APOC3 similarly been revealed to assist hepatic VLDL emission and assembly. It is not only a main TRLs modulator but similarly participates to the atherogenicity of HDL and LDL molecules [20]. Clear data show that APOC3 has a number of further roles, involving irritation and endothelial function modulation [21]. The association of APOC3 with high levels of TG and CVD risk has been established in broad humans and animal data [22]. Additionally, assumed that TRL fragments are currently documented as an underlying danger issue for CVD and that damage APOC3 function mutations which described by a strong dropping of serum TG and decreased the danger of CVD [23, 24].
Neutrophil elastase (NE) is a powerful serine protease that has specificity of extensive substrate [25]. Investigational data have possibly dealt with the damaging nature of NE, but a previous paper shows that NE can irritate a diversity of proinflammatory replies, like TGF manufacture in smooth muscle c
