The aim of this study was to analyze the changes of interleukin-6 (IL-6), C-reactive protein (CRP), blood lipids and myocardial indexes after treatment of patients with acute myocardial infarction (AMI) with intensive atorvastatin and interventional therapy, and its clinical significance.
We aimed to investigate changes in the levels of cytokines (IL-6, TNF-α and IL-10), miRNAs profiles (miR-146 and miR-155) and distribution of different monocyte subsets (CD14++CD16-, CD14++CD16+, CD14+CD16++) in the acute and post-healing phases of AMI.
Treatment with dabigatran significantly inhibited the P65 of nuclear factor κB, tumor necrosis factor α, interleukin (IL)‑1β and IL‑6 activities and significantly enhanced the catalase and superoxide dismutase activities in the AMI rabbits.
Here we investigated products of complement activation, C3d and soluble C5b9 (sC5b9), as potential biomarkers for myocardial injury and inflammation, as well as serum cytokines (IL-6 and TNF-alpha), alpha-1-acid glycoprotein (AGP), and classical markers of myocardial necrosis (creatine kinase, creatine kinase-MB isoform, myoglobin and troponin-I) in a longitudinal study of patients with AMI (from admission, 6 h and 12 h post admission, and at discharge from hospital).
In the present study, western blotting was used to verified the expression of T lymphocyte CaSR and pathway proteins, including phosphorylated extracellular signal‑regulated kinase (P‑ERK)1/2 and phosphorylated c‑Jun N‑terminal kinase (P‑JNK), and used cytometric bead array to detect the secretion of interleukin (IL)‑4, IL‑6, IL‑10 and tumor necrosis factor (TNF)‑α in AMI onset, the results demonstrated that they were all increased.
We measured serum activated protein C and interleukin-6 levels in 43 patients with cardiogenic shock following acute myocardial infarction and in 15 control patients with uncomplicated myocardial infarction at days 0-5 and 7 after the onset of shock/myocardial infarction.
Diethylcarbamazine treatment significantly weakened reactive oxygen species production and reduced the levels of tumor necrosis factor (TNF)‑α, interleukin‑6 and NF‑κB/p65 in AMI rats.
ELISA analysis shows that serum concentrations of VEGF and inflammatory factor IL-1β, TNF-α and IL-6 were increased in AMI patients compared to a control group.
PB interleukin-6 (IL-6) negatively correlated with endothelial colony-forming cell colony maximum in the BM of patients with AMI (estimate±SE, -0.13±0.05; <i>P</i>=0.007).
The results of the present study demonstrated that circulating hepcidin-25 and IL-6 were both elevated in the acute phase of MI and that hepcidin-25 released from plaque macrophages and other cell sources contributed to the plaque instability by inducing endothelial cell death.
The findings indicated that diminazene significantly reduced the levels of inflammatory factors including tumor necrosis factor‑α and interleukin‑6, suppressed the protein expression of cytochrome c oxidase subunit 2 (COX‑2) and inducible nitric oxide synthase (iNOS), and activated angiotensin‑converting enzyme 2 (ACE2), angiotensin II receptor type 1 (AT1R) and MAS1 proto‑oncogene, G protein‑coupled receptor (MasR) protein expression in AMI model rats.
Serum interleukin-6 levels in patients with AMI were significantly higher than nonischemic controls (0.4 ± 0.2 ng/mL versus 0.2 ± 0.07 ng/mL, respectively, P = 0.03).
The results of our study revealed that inflammatory cytokines IL-6 and TNF-<i>α</i> induce cardiac remodeling in rats after AMI; HMP improves cardiac function and ameliorates ventricular remodeling by downregulating the expression of IL-6 and TNF-<i>α</i> and further suppressing the ultrastructural changes of myocardial cells.
The increased KIM-1 and NGAL expression levels after MI in the OLETF kidney were associated with upregulated expression of TLR1, TLR2, TLR4, MyD88, IL-6, TNF-α, chemokine (C-C motif) ligand 2, and transforming growth factor-β<sub>1</sub> and also with activation of p38 MAPK, JNK, and NF-κB.
The IL6 -174G>C and CD14 -260C>T polymorphisms are likely to be associated with a pro-atherogenic profile but not with increased inflammatory markers and endothelial dysfunction in young AMI patients.
The aim of this study was to investigate whether molecular polymorphism of the IL-6 gene is involved in the predisposition to acute myocardial infarction (AMI).