Atherosclerosis is an inflammatory disease involving activation of adaptive and innate immune responses to antigens, including oxidized low-density lipoprotein (oxLDL) and phosphorylcholine (PC). Dendritic cells (DCs), which are antigen-presenting cells that activate T cells, are present in atherosclerotic lesions and are activated in immune organs. However, the mechanism by which PC promotes atherosclerosis is unclear.
View Article and Find Full Text PDFOxidative stress and subsequent cardiac myocyte apoptosis play central roles in the initiation and progression of myocardial ischemia-reperfusion (I/R) injury. Homeobox transcript antisense intergenic RNA () was previously implicated in various heart diseases, yet its role in myocardial I/R injury has not been clearly demonstrated. Mice with cardiac-restricted knockdown or overexpression of were exposed to I/R surgery.
View Article and Find Full Text PDFBACKGROUND Malvidin (alvidin-3-glucoside) is a polyphenol that belongs to the class of natural anthocyanin, which is abundantly found in red wines, colored fruits, and the skin of red grapes. Therefore, the current investigation was intended to evaluate the effect of malvidin against myocardial infarction induced by isoproterenol in the rats. MATERIAL AND METHODS The cardioprotective effects was assessed by determining the effect of malvidin on the activities of endogenous antioxidants - catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH) - and on the levels of lipid peroxidation and serum marker enzymes.
View Article and Find Full Text PDFBackground/aims: Myeloid-derived suppressor cells (MDSCs) are increased in inflammatory and autoimmune disorders. This study aims to evaluate the significance of MDSCs in dilated cardiomyopathy (DCM) patients.
Methods: In total, 42 newly hospitalized DCM patients and 39 healthy controls were enrolled in the study.
Cell Physiol Biochem
September 2015
Aim: The aim of this study was to explore whether the circulating frequency and function of myeloid-derived suppressor cells (MDSCs) are altered in patients with acute coronary syndrome (ACS).
Methods: The frequency of MDSCs in peripheral blood was determined by flow cytometry, and mRNA expression in purified MDSCs was analyzed by real-time reverse transcription polymerase chain reaction (RT-PCR). The suppressive function of MDSCs isolated from different groups was also determined.
Objective: To investigate the role of CD4(+)CD25(+) T cells (Tregs) in protecting fine particulate matter (PM-) induced inflammatory responses, and its potential mechanisms.
Methods: Human umbilical vein endothelial cells (HUVECs) were treated with graded concentrations (2, 5, 10, 20, and 40 µg/cm(2)) of suspension of fine particles for 24h. For coculture experiment, HUVECs were incubated alone, with CD4(+)CD25(-) T cells (Teff), or with Tregs in the presence of anti-CD3 monoclonal antibodies for 48 hours, and then were stimulated with or without suspension of fine particles for 24 hours.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
August 2011
Aim: To investigate the correlation between the levels of serum IFN-γ and RANTES (regulated upon on activation on normal T cell expressed and secreted) and rabbit atherosclerotic plaque stability.
Methods: 30 male New Zealand rabbits were randomly divided into three groups: control group, stable atherosclerotic plaque group(AS group) and vulnerable atherosclerotic plaque group(VAP group), with 10 rabbits in a group. The control group was given normal diet while the AS group and the VAP group were given high-fat diet for 12 weeks.
Many studies have suggested that VSMC (vascular smooth muscle cell) apoptosis plays a key role in destabilization and rupture of atherosclerotic plaques. Therefore protection for VSMCs from apoptosis is a promising approach to stabilize 'vulnerable' lesions. However, the mechanisms as to why VSMCs in the fibrous cap often appear as profilerated in early stages, but turn apoptotic in advanced stages, are still unknown.
View Article and Find Full Text PDFBackground And Aims: There is an imbalance between Th1 and Th2 in the development and progression of atherosclerosis and in patients with acute coronary syndrome (ACS) including acute myocardial infarction (AMI) and unstable angina. T helper cell type 3 (Th3), which primarily secretes transforming growth factor beta-1 (TGF-beta1), has been shown to inhibit both Th1 and Th2 cells. The present study was designed to investigate whether Th3 cells are involved in plaque destabilization and the onset of ACS.
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