Interleukin-6 and Cardiovascular Diseases

Inflammation is a major risk factor for cardiovascular complications. Magnesium sulfate (MgSO4) has anti-inflammatory actions. Therefore we investigated the effects of levothyroxine and MgSO4 on inflammatory markers as C-reactive protein (CRP), interleukin-6, tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in hypothyroid rats. Sixty male rats were divided into 6 groups; normal, normal + MgSO4, hypothyroidism, hypothyroidism + levothyroxine, hypothyroidism + MgSO4, and hypothyroidism + levothyroxine + MgSO4. Thyroxine, triiodothyronine, and thyroid-stimulating hormone (TSH), CRP, interleukin-6, TNF-α, ICAM-1, and VCAM-1 were measured in all rats. Hypothyroidism significantly increased TSH, CRP, interleukin-6, TNF-α, ICAM-1, and VCAM-1 and decreased triiodothronine and thyroxine. Treatment of hypothyroid rats with levothyroxine or MgSO4 significantly decreased CRP, interleukin-6, TNF-α, ICAM-1, and VCAM-1. Combined therapy of hypothyroid rats with levothyroxine and MgSO4 significantly decreased CRP, interleukin-6, TNF-α, ICAM-1, and VCAM-1 compared with hypothyroid rats either untreated or treated with levothyroxine or MgSO4. This study demonstrates that hypothyroid rats have chronic low grade inflammation, which may account for increased risk of cardiovascular diseases. Combined levothyroxine and MgSO4 is better than levothyroxine or MgSO4 alone in alleviating the chronic low grade inflammatory status and therefore reducing the risk of cardiovascular diseases in hypothyroid animals.

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Circulating interleukin-1β and interleukin-6 concentrations are closely associated with γ-glutamyltranspeptidase activity in middle-aged Japanese men without obvious cardiovascular diseases

Metabolism ◽

10.1016/j.metabol.2010.08.011 ◽

2011 ◽

Vol 60 (7) ◽

pp. 914-922 ◽

Cited By ~ 4

Author(s):

Kazuki Mochizuki ◽

Yasumi Misaki ◽

Rie Miyauchi ◽

Satsuki Takabe ◽

Masaya Shimada ◽

...

Keyword(s):

Cardiovascular Diseases ◽

Interleukin 6 ◽

Interleukin 1Β ◽

Middle Aged ◽

Japanese Men

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Peculiarities of the Immune Status of Petrochemical Workers with Cardiovascular Diseases

ЗДОРОВЬЕ НАСЕЛЕНИЯ И СРЕДА ОБИТАНИЯ - ЗНиСО / PUBLIC HEALTH AND LIFE ENVIRONMENT ◽

10.35627/2219-5238/2020-326-5-47-51 ◽

2020 ◽

pp. 47-51

Author(s):

Yu.A. Chelakova ◽

O.V. Dolgikh

Keyword(s):

Monoclonal Antibodies ◽

Cardiovascular Diseases ◽

Interleukin 6 ◽

Reference Group ◽

Specific Antigen ◽

Test Group ◽

Annexin V ◽

The Body ◽

Enzyme Linked Immunosorbent Assay ◽

Effector Cells

Objective: The purpose of our research was to assess characteristics of immune regulation in petrochemical workers suffering from cardiovascular diseases (CVD). Materials and methods: Our sample was divided into two groups: an observation group consisting of 115 people with CVD and a reference group of 56 people. Blood benzene was assayed by gas chromatography. Cellular phagocytosis was examined using formalinized sheep erythrocytes. The IgG content specific to benzene was measured using the allergosorbent test. CD-lymphocytes were phenotyped on a flow cytometer via membrane immune fluorescence and applying a panel of labeled monoclonal antibodies to membrane CD-receptors. Expression of TNFR, p53, Bcl-2, and bax was determined by applying relevant monoclonal antibodies. We used the enzyme-linked immunosorbent assay (ELISA) to determine total IgG, CA 19-9, prostate-specific antigen (PSA), interleukin-6, and VEGF. Statistical data analysis was performed using techniques of descriptive statistics and sample comparison. Intergroup differences were considered statistically significant at р≤0.05. Results: Chemical analytical tests revealed an excess benzene burden in the test group against the reference one. Immunoassays showed higher cellular phagocytic activity. We detected significant changes in CD-immunogram parameters such as increased concentrations of CD16+ effector cells, activation of Т-suppressors lymphocytes CD127-, an increase in Annexin V-FITC+7ADD-negative cells, TNFR, p53, bcl-2, bax, as well as the deficiency of CD19+, CD25+, CD95+ lymphocytes both against the reference group and physiological standards. We also determined an increase in total and benzene-specific sensibilization of the body, elevated concentrations of tumor markers CA 19-9 and PSA, interleukin-6, and the growth factor of vessels endothelium VEGF. All these changes characterized the features of immune homeostasis indicators and were responsible for pathogenesis and development of cardiovascular diseases. Conclusions: Significant associations of immunologic parameters in the form of functional disorders in programmed cells death with simultaneous activation of specific sensibilization processes create specific immunologic status of petrochemical workers with cardiovascular diseases in their medical history.

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Role of serum interleukin-6 in heart failure

International Journal of Advances in Medicine ◽

10.18203/2349-3933.ijam20183123 ◽

2018 ◽

Vol 5 (4) ◽

pp. 936 ◽

Cited By ~ 1

Author(s):

Smita Amol Deokar ◽

Sucheta P. Dandekar ◽

Ganesh A. Shinde ◽

Surekha S. Prabhu ◽

Mugdha Patawardhan

Keyword(s):

Heart Failure ◽

Cardiovascular Disease ◽

Cardiovascular Diseases ◽

Interleukin 6 ◽

Inflammatory Marker ◽

Serum Analysis ◽

Heart Failure Patients ◽

Growing Body ◽

Age And Sex

Background: A growing body of evidence suggests that inflammation plays the key role in different cardiovascular diseases. But very study has been done so far in relation to serum interleukin-6 in heart failure patients. The aim of the study was to measure serum interleukin-6 in heart failure patients.Methods: Total 22 heart failure patients and 22 age and sex matched controls were included in this study from August 2015 to June 2016 for serum analysis of interleukin-6.Results: serum interleukin-6 was significantly [median(IQR) 14.3(26.2) pg/mL] increased in heart failure patients compared to age and sex matched controls [median(IQR) 0(2.4) pg/mL].Conclusions: Even though little is known about function of interleukin-6 in heart failure patients, this study shows that increased level of IL-6 in heart failure patients plays an important role as a pro-inflammatory marker in development of cardiovascular disease i.e. heart failure.

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Inflammageing in the cardiovascular system: mechanisms, emerging targets, and novel therapeutic strategies

Clinical Science ◽

10.1042/cs20191213 ◽

2020 ◽

Vol 134 (17) ◽

pp. 2243-2262

Author(s):

Danlin Liu ◽

Gavin Richardson ◽

Fehmi M. Benli ◽

Catherine Park ◽

João V. de Souza ◽

...

Keyword(s):

Cardiovascular Diseases ◽

Cardiovascular System ◽

Nlrp3 Inflammasome ◽

Molecular Mechanisms ◽

Molecular Targets ◽

Therapeutic Interventions ◽

Low Grade ◽

Cardiovascular Research ◽

Inflammatory Processes ◽

Ach Receptors

Abstract In the elderly population, pathological inflammation has been associated with ageing-associated diseases. The term ‘inflammageing’, which was used for the first time by Franceschi and co-workers in 2000, is associated with the chronic, low-grade, subclinical inflammatory processes coupled to biological ageing. The source of these inflammatory processes is debated. The senescence-associated secretory phenotype (SASP) has been proposed as the main origin of inflammageing. The SASP is characterised by the release of inflammatory cytokines, elevated activation of the NLRP3 inflammasome, altered regulation of acetylcholine (ACh) nicotinic receptors, and abnormal NAD+ metabolism. Therefore, SASP may be ‘druggable’ by small molecule therapeutics targeting those emerging molecular targets. It has been shown that inflammageing is a hallmark of various cardiovascular diseases, including atherosclerosis, hypertension, and adverse cardiac remodelling. Therefore, the pathomechanism involving SASP activation via the NLRP3 inflammasome; modulation of NLRP3 via α7 nicotinic ACh receptors; and modulation by senolytics targeting other proteins have gained a lot of interest within cardiovascular research and drug development communities. In this review, which offers a unique view from both clinical and preclinical target-based drug discovery perspectives, we have focused on cardiovascular inflammageing and its molecular mechanisms. We have outlined the mechanistic links between inflammageing, SASP, interleukin (IL)-1β, NLRP3 inflammasome, nicotinic ACh receptors, and molecular targets of senolytic drugs in the context of cardiovascular diseases. We have addressed the ‘druggability’ of NLRP3 and nicotinic α7 receptors by small molecules, as these proteins represent novel and exciting targets for therapeutic interventions targeting inflammageing in the cardiovascular system and beyond.

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