期刊
CURRENT ISSUES IN MOLECULAR BIOLOGY
卷 43, 期 2, 页码 704-715出版社
MDPI
DOI: 10.3390/cimb43020051
关键词
3-nitrotyrosine (NT); asymmetric dimethylarginine (ADMA); cardiovascular disease; coenzyme Q10 (CoQ10); inflammasome; peripheral blood mononuclear cells (PBMC); periodontitis (PT)
This study found that patients with cardiovascular disease and periodontitis share common risk factors, with plasma biomarkers related to inflammatory status in these patients; certain gene expression levels in peripheral blood mononuclear cells were significantly up-regulated in patient groups. This suggests a possible link between oxidative stress, inflammasome activation, and endothelial dysfunction in periodontitis patients leading to the pathogenesis and progression of coronary heart disease.
Patients with cardiovascular disease (CVD) and periodontitis (PT) show shared risk factors as result of the altered molecular mechanisms associated with pathological conditions. The aim of our study was to evaluate if the plasma biomarkers associated with endothelial dysfunction may also be related to alterations in the inflammatory status in peripheral blood mononuclear cells (PBMC). Patients with PT, coronary heart disease (CHD), or both diseases as well as controls were enrolled. Plasma levels of coenzyme Q10 (CoQ10), 3-nitrotyrosine (NT), and asymmetric dimethylarginine (ADMA) were assessed using HPLC. mRNA levels of caspase-1 (CASP1), NLR family pyrin domain containing 3 (NLRP3), and tumor necrosis factor-alpha (TNF-alpha) in PBMC from the recruited subjects were quantified using real-time PCR. Patients with PT + CHD showed lower CoQ10 plasma levels and increased concentrations of NT in comparison to healthy subjects. ADMA levels were higher in CHD and PT + CHD patients compared to controls. Transcript levels of CASP1, NLRP3, and TNF-alpha were up-regulated in PBMC from all patient groups when compared to healthy subjects. Our results suggest a possible causal link between oxidative stress, high levels of NT and ADMA, and inflammasome activation, which may be involved in the endothelial inflammatory dysfunction leading to the pathogenesis and progression of CHD in PT patients.
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