Correlation Pattern of oxLDL, cortisol, hsCRP, and Adiponectin Levels in Atherosclerosis Risk Population-Based on Framingham Risk Score

Kumboyono, Kumboyono; Chomsy, Indah Nur; Aini, Fitria Nugraha; Wihastuti, Titin Andri

doi:10.5530/pj.2022.14.3

Cited by 4 publications

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“…Cotinine level, nAChRs, and Tie2 measurements were conducted by centrifuging the blood for 15 min at a speed of 2000-3000 rpm at a temperature of 2-8 o C to collect the plasma. Then, the samples were analyzed using the ELISA Kit to determine the levels of cotinine (Human Cotinine, Bioassay Technology Laboratory, E2043Hu), nAChRs (Human Nicotinic Acetylcholine Transferase Receptor, Bioassay Technology Laboratory, E1330Hu), Tie2 (Human Tyrosine Kinase with Immunoglobulinlike and EGF-like Domains 2, Bioassay Technology Laboratory, E1219Hu) 15 .…”

Section: Enzyme-linked Immunosorbent Assay To Analyze the Level Of Co...mentioning

confidence: 99%

Nicotine is associated with smoking dependence and vascular inflammation through cotinine: A mediation analysis

Kumboyono,

Chomsy,

Shalshabilla

et al. 2024

Tob. Induc. Dis.

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INTRODUCTION The main alkaloid component in cigarettes is nicotine. Cotinine, a metabolite of nicotine, is capable of causing dependence effects through endless mechanisms modulated by the ion channel nicotinic acetylcholine receptors nAChRs. Nicotine and cotinine can also cause damage to blood vessels through a chronic inflammatory process mediated by the Ligand-Tie2 Angiopoietin Receptor system. Hypoxic conditions that occur due to vascular inflammation cause a decrease in the concentration of nitric oxide (NO). This study aimed to evaluate the relationship between NO levels and cotinine through the expression of nAChRs that mediate the nicotine dependence mechanism and Tie2 (Tyrosine Kinase 2) expression. METHODS A cross-sectional study was conducted with 200 participants grouped into two groups based on their smoking status: 100 smokers and 100 non-smokers. All participants were men aged 20-40 years with no history of cardiovascular disease, diabetes mellitus, or dyslipidemia, and were not currently on medication. According to the parameters used, all blood samples were taken from peripheral blood for analysis using the ELISA kit or Colorimetric Assay Kit. RESULTS Cigarette consumption increases blood cotinine concentrations in smokers and causes dependence by modulating nAChRs. The study indicates an emerging cycle regarding nicotine-cotinine consumption and nAChRs expression. In addition, the data in this study showed a significant relationship (p<0.001) regarding the cycle formed with decreased NO levels as a result of damage caused by Tie2-mediated inflammation. CONCLUSIONS There is a relationship between NO levels and cotinine through nAChRs, which mediate the nicotine dependence mechanism and Tie2 expression.

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Section: Enzyme-linked Immunosorbent Assay To Analyze the Level Of Co...mentioning

confidence: 99%

Nicotine is associated with smoking dependence and vascular inflammation through cotinine: A mediation analysis

Kumboyono,

Chomsy,

Shalshabilla

et al. 2024

Tob. Induc. Dis.

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“…However, until now, the exact cause of this disease is unknown, but the presence of risk factors is known to trigger the emergence of this disease often. The critical factor that causes this disease to appear is when LDL (low-density lipoprotein) cholesterol is oxidized (ox-LDL), which is then phagocytosed by macrophages to form foam cells [2,3]. This condition then becomes one of the causes of atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Nanoparticles–SIRT1 Prevents Endothelial Progenitor Cells Senescence by Modulating Nitric Oxide Expression and Reducing Poly ADP-ribose Polymerase: In vitro Study

Wihastuti,

Chomsy,

Nurwidyaningtyas

et al. 2024

Trends Sci

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One of cardiovascular diseases that accounts for a high global death rate is atherosclerosis. Apart from the known risk factors, the cause of this disease is uncertain. This disease is triggered by the rupture of atheroma. This condition is associated with oxidative stress, which can trigger endothelial progenitor cells (EPC) dysfunction. One of the causes of oxidative stress is hydrogen peroxide, which triggers deoxyribose nucleotide acid (DNA) damage, which will later trigger ageing in EPC. Sirtuin-1 (SIRT1) is known to be involved in EPC repair, but currently, no studies have attempted to increase SIRT1 expression in vitro. This study aimed to determine the effect of nanoparticles-SIRT1 (NPS1) on the expression of nitric-oxide (NO) and poly (ADP-ribose)-polymerase (PARP) in EPC cell cultures induced by hydrogen peroxide (H2O2). Tests were carried out in vitro using EPC cell cultures to determine the potential of SIRT1 (NPS1) nanoparticles as an ageing inhibitor. The research method used was pure quantitative experimental with a post-test-only control group. The expression of NO and PARP was studied using the flow cytometry method. The data obtained were analysed using parametric one-way ANOVA and post-hoc Tukey-HSD tests with a 95 % confidence interval (p ≤ 0.05). The results showed that administration of SIRT1 nanoparticles was able to increase NO expression in EPC culture cells that induced H2O2 by 14.61 % and could also increase NO levels in normal EPC cells that were only given NPS1 by 38.51 % and was able to reduce PARP expression when compared with the normal group. The NPS1 given was 9.03 % for the NPS1 group and 19.78 % for the NPS1+ H2O2 group. This study concludes that NPS1 added to EPC cells further helps increase cell repair to prevent senescence, through increasing NO and also increasing the performance of PARP. HIGHLIGHTS This study aims to determine the effect of Sirtuin-1 (SIRT1) nanoparticles on nitric oxide (NO) and poly (ADP-ribose)-polymerase (PARP) expression in their role as senescence blockers in endothelial progenitor cells (EPC) by maintaining SIRT1 levels to keep EPC cells alive and functioning optimally This research succeeded in modulating NO levels with a significant increase in NO. This study found that Nanoparticles–SIRT1 (NPS1) added to EPC cells further helps increase cell repair to prevent senescence, through increasing NO and also increasing the performance of PARP as an enzyme that functions in the DNA repair response at levels that are not excessive and does not exceed SIRT1 levels in cells. GRAPHICAL ABSTRACT

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“…In adolescents, smoking becomes a severe problem when they start smoking in their teens, which will cause nicotine addiction and be difficult to quit [4]. Smoking behaviour hurts blood vessels in the form of inflammation with endothelial activation that forms a pattern of pathological adaptation [16]. Another influence on endothelial cells in smokers, namely smoking behaviour, causes endothelial progenitor cells to age by showing dysfunction in the EPC, which results in a decrease in angiogenic cell function impact on the haematological system [17].…”

Section: Introductionmentioning

confidence: 99%

Differences in Haemoglobin and Erythrocytes Levels in Smokers and Non-smokers

Kumboyono¹,

Anggara²,

Agustina³

et al. 2023

Advances in Economics, Business and Management Research

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Smoking is the cause of various health problems. The prevalence of smokers continues to increase due to the content of addictive substances in cigarettes, such as tobacco, tar, and nicotine. This addictive substance in nicotine causes adverse effects on various organ systems. Several studies have stated a link between blood components and smokers, as evidenced by the relationship between nicotine levels and blood components. This study aims to determine the relationship between nicotine and its metabolite levels and smokers' Haemoglobin and erythrocytes levels. The study used an analytic observational design, and the approach used was cross-sectional. Samples were taken using the total sampling technique and considering the research criteria. The research sample was 57 people, consisting of 34 smokers and 23 non-smokers in Malang City. The level of nicotine and its metabolites is a significant variable; the dependent variable is the level of Haemoglobin and erythrocytes. Demographic data collection using a google form questionnaire. Variable data on nicotine and its metabolites were measured using the Human Cotinine ELISA Kit instrument, and varying levels of Haemoglobin and erythrocytes using the Cobas Micros tool. Pearson Correlation test was used on the results of data analysis. The correlation between cotinine and Haemoglobin (p-value) is 0.981, and cotinine and erythrocytes (p-value) are 0.313. Each has a p-value > 0.05; therefore, it is concluded that smokers have no association between nicotine levels and its metabolites with Haemoglobin and erythrocytes levels. Based on the results of this study, people better understand the dangers of smoking and prevent smoking behaviour.

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Correlation Pattern of oxLDL, cortisol, hsCRP, and Adiponectin Levels in Atherosclerosis Risk Population-Based on Framingham Risk Score

Cited by 4 publications

References 0 publications

Nicotine is associated with smoking dependence and vascular inflammation through cotinine: A mediation analysis

Nicotine is associated with smoking dependence and vascular inflammation through cotinine: A mediation analysis

Nanoparticles–SIRT1 Prevents Endothelial Progenitor Cells Senescence by Modulating Nitric Oxide Expression and Reducing Poly ADP-ribose Polymerase: In vitro Study

Differences in Haemoglobin and Erythrocytes Levels in Smokers and Non-smokers

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