Comparison of serum levels of IL-6, IL-8, TGF-β and TNF-α in coronary artery diseases, stable angina and participants with normal coronary artery

2018 ◽  
Vol 64 (5) ◽  
pp. 1 ◽  
Author(s):  
Zahra Sepehri Sepehri ◽  
Mohammad Masoomi ◽  
Fatemeh Ruzbehi ◽  
Zohreh Kiani ◽  
Ali Akbar Nasiri ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Stable Angina ◽  
Serum Levels ◽  
Normal Coronary Artery ◽  
Coronary Artery Diseases ◽  
Tnf Α

scholarly journals IL-32 Serum Levels in Coronary Artery Disease Patient and its Relationship with IL-6 and TNF-α Serum Levels

2021 ◽  
Author(s):  
Mina Mohammad-Rezaei ◽  
Reza Ahmadi ◽  
Ali Rafiei ◽  
Arsalan Khaledifar ◽  
Shohila Fatahi ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Serum Levels ◽  
Arterial Stenosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Subjects ◽  
Tnf Α ◽  
Significant Difference ◽  
Major Vessel ◽  
Artery Disease

Abstract Coronary Artery Disease (CAD) is a chronic inflammatory disease caused by atherosclerosis and arteries become clogged due to plaque formation, fat accumulation, and various sorts of immune cells. IL-32 is a new proinflammatory cytokine, which enhances inflammation through inducing different inflammatory cytokines. The purpose of current research was to assess IL-32 serum levels in coronary artery disease subjects and its relationship with serum levels of IL-6 and TNF-α. Forty-two subjects diagnosed with CAD and thirty-nine control subjects were enrolled in the research. Serum levels of IL-6, TNF-α, and IL-32 were measured using the enzyme-linked immunosorbent assay (ELISA). IL-32, TNF-α, and IL-6 serum levels were significantly higher by 2.7, 3.48, and 3.2-fold in the CAD subjects than in control subjects, respectively. Moreover, no significant difference was found in TNF-α, IL-6 and IL-32 serum levels with the clogged arteries number in the CAD group. TNF-α and IL-32 serum levels in the CAD subjects with cardiac arterial stenosis in one major vessel were significantly increased than CAD subjects with cardiac arterial stenosis in more than one major vessels. ROC curve analysis revealed that serum levels of IL-32, TNF-α, and IL-6 showed good abilities in predicting CAD. Also, Multiple logistic regression analyses suggested that TNF-α, IL-6, and IL-32, serum levels of LDL and ox-LDL were independently related to the presence of CAD, while HDL serum levels were not. TNF-α, IL-32, and IL-6 showed an increase in CAD group and serum levels of these cytokines showed good abilities in predicting CAD. Our data suggested the involvement of TNF-α and IL-32 in the early stage of CAD.

scholarly journals Levels of pregnancy-associated plasma protein A in patients with coronary artery disease

2008 ◽  
Vol 31 (2) ◽  
pp. 85 ◽  
Author(s):  
Zhi-Yuan Liu ◽  
Jin-Ying Zhang ◽  
Tong-Wen Sun ◽  
Yan-Jun Zhang ◽  
Li Zhang ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Plasma Protein ◽  
Stable Angina ◽  
Protein A ◽  
Serum Levels ◽  
Control Group ◽  
Coronary Syndrome ◽  
Artery Disease

Purpose: To investigate the levels of pregnancy-associated plasma protein A (PAPP-A) or insulin-like growth factor -1 (IGF-1) in patients with acute coronary syndrome. Methods: Serum PAPP-A and IGF-1 was measured with biotin–tyramide-amplified enzyme immunoassay and Enzyme Linked Immuoserbent Assay, respectively, in patients with ST elevation acute myocardial infarction (STEMI, n=12), unstable angina (UAP, n=15), and stable angina (n=15). PAPP-A and IGF-1 was also measured in 16 healthy subjects (control group). Results: The serum levels of PAPP-A in the STEMI (16.9±10.3 mIU/L) and UAP group (15.2±10.5 mIU/L) were higher than in the stable angina (8.5±3.1 mIU/L) or control group (8.4±2.0 mIU/L, P < 0.01). The serum levels of IGF-1 in the STEMI (132.3±40.9 µg/L) and UAP group (127.3±36.0 µg/L) were also higher than in the stable angina (44.9±18.5 µg/L) or control group (67.7±24.5µg/L, P < 0.01). There were no differences in serum levels of PAPP-A or IGF-1 among the single, double and three vessel lesion groups. The serum levels of PAPP-A (19.9±10.1 mIU/L) and IGF-1 (153.2±52.4 µg/L) after PCI were higher than those before PCI (15.1±10.0 mIU/L and 91.4±51.0 µg/L, respectively, P < 0.01). A positive correlation was found between PAPP-A and IGF-1 levels in the STEMI and UAP group before PCI (r=0.48?P < 0.01). Conclusion: PAPP-A and IGF-1 are elevated in patients with acute coronary syndrome. They may be used as biomarkers for vulnerable plaques in patients with coronary artery disease. Whether post-PCI elevation of IGF-1 can be used to predict restenosis of coronary arteries remains to be seen.

Serum levels of IL-32 in patients with coronary artery disease and its relationship with the serum levels of IL-6 and TNF-α

2021 ◽  
Author(s):  
Mina Mohammad-Rezaei ◽  
Reza Ahmadi ◽  
Ali Rafiei ◽  
Arsalan Khaledifar ◽  
Soheila Fattahi ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Serum Levels ◽  
Tnf Α ◽  
Artery Disease

scholarly journals Serum levels of Asprosin in patients diagnosed with coronary artery disease (CAD): a case-control study

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Nariman Moradi ◽  
Fatima Zahraa Fouani ◽  
Akram Vatannejad ◽  
Abbas Bakhti Arani ◽  
Soraya Shahrzad ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Polycystic Ovary ◽  
Serum Levels ◽  
Type Ii Diabetes Mellitus ◽  
Chronic Inflammatory Disease ◽  
Increased Risk ◽  
Tnf Α ◽  
Artery Disease ◽  
Control Study

Abstract Background Coronary artery disease (CAD) is considered as a multi-faceted chronic inflammatory disease involving reduced blood supply to the myocardium as a result of accumulating lipids in the atrial walls. Visceral adiposity with disrupted release of adipokines play a key role in its pathogenesis. Asprosin is a newly identified fasting-induced glucogenic adipokine that has been related with metabolic disorders such as type II diabetes mellitus and polycystic ovary syndrome. The preset study sought to assess circulating asprosin in context of CAD. Methods In this study, serum levels of asprosin were determined in 88 CAD patients and 88 non-CAD healthy controls. Serum IL-6, TNF-α, asprosin and adiponectin were assessed using ELISA kits. Results: Serum asprosin was found to be higher in CAD patients when compared to non-CAD subjects (7.84 ± 2.08 versus 5.02 ± 1.29 μg/mL, p <  0.001). Similarly, serum TNF-α, and IL-6 elevated in CAD group significantly (p <  0.001). However, circulating adiponectin diminished in CAD group when compared with non-CAD subjects (p < 0.001). Moreover, serum asprosin levels directly correlated with BMI, FBG, HOMA-IR, TG and TC. Logistic regression analyses showed that asprosin levels were associated with increased risk of developing CAD (odds ratio: 3.01, 95% CI: 2.16, 4.20 and p < 0.001), after adjusting for potential confounders (age, sex and BMI). Conclusions The present study findings suggested a possible relation of serum asprosin with the pathogenesis of CAD, in particular through insulin resistance and dyslipidemia.

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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