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Teuku Heriansyah,1 Herlina Dimiati,1 Tjut Farahiya Hadi,1 Dimas Arya Umara,1 Lian Varis Riandi,2 Fauzan Fajri,3 Sukmawan Fajar Santosa,4 Titin Andri Wihastuti,5 Kumboyono Kumboyono6 1Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Syiah Kuala, Banda Aceh, Aceh, Indonesia; 2Department of Parasitology, Faculty of Veterinary Medicine, Universitas Syiah Kuala, Banda Aceh, Aceh, Indonesia; 3Department of Animal Model, Faculty of Veterinary Medicine, Universitas Syiah Kuala, Banda Aceh, Aceh, Indonesia; 4Integrated Research Laboratory, Faculty of Veterinary Medicine, Universitas Syiah Kuala, Banda Aceh, Aceh, Indonesia; 5Department of Basic Nursing, Faculty of Health Sciences, Universitas Brawijaya, Malang, Jawa Timur, Indonesia; 6Department of Nursing, Faculty of Health Sciences, Universitas Brawijaya, Malang, IndonesiaCorrespondence: Tjut Farahiya Hadi, Email tjut@mhs.unsyiah.ac.idIntroduction: Ascorbic acid and calcitriol were frequently utilized in conjunction as therapy during the COVID-19 pandemic, and individuals with minor symptoms had notable improvements. There have been a few studies, often with conflicting findings, that examine the use of them for endothelium restoration and numerous clinical trial studies that failed to establish the efficacy. The aim of this study was to find the efficacy of ascorbic acid compared to calcitriol on the inflammatory markers monocyte chemoattractant protein-1 (MCP-1), nitric oxide (NO), and superoxide dismutase (SOD), as protective agents which play an important role in the early stages of atherosclerosis formation. This study was an experimental in vivo study.Methods: The total of 24 male Rattus norvegicus strain Wistar rats were divided into 4 groups, namely: control/normal group (N), atherosclerosis group (DL) given atherogenic diet, atherosclerosis group given atherogenic diet and ascorbic acid (DLC), and atherosclerosis group given atherogenic diet and calcitriol (DLD) treatment for 30 days.Results: Ascorbic acid and calcitriol treatment was significantly effective (P< 0.05) in lowering expression of MCP-1 and increasing NO and SOD level. Calcitriol was superior to ascorbic acid in increasing SOD (P< 0.05). There was no significant difference between ascorbic acid and calcitriol in decreasing MCP-1 and increasing NO (P> 0.05).Discussion: Both treatments could reduce MCP-1, and increase NO and SOD by increasing antioxidants. In this study calcitriol was superior to ascorbic acid in increasing SOD, but not NO and decreasing MCP-1. According to the theory, it was found that calcitriol through nuclear factor erythroid 2-related factor 2 (Nrf2) causes a direct increase in the amount of SOD. Nrf2 is an emerging regulator of cellular resistance to oxidants.Conclusion: Ascorbic acid and calcitriol treatment was able to reduce MCP-1 and increase NO and SOD in atherosclerosis rat. Calcitriol was significantly superior in increasing SOD levels compared to ascorbic acid.Keywords: ascorbic acid, calcitriol, monocyte chemoattractant protein-1, nitric oxide, superoxide dismutase, atherosclerosis

Kumboyono Kumboyono,1 Wiwit Nurwidyaningtyas,2 Indah Nur Chomsy,2 Titin Andri Wihastuti3 1Nursing Department, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia; 2Doctoral Program of Medical Science, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia; 3Department of Biomedicine, Faculty of Medicine, University of Brawijaya, Malang, 65145, IndonesiaCorrespondence: Kumboyono Kumboyono Email publikasikoe@gmail.comIntroduction: Smoking can cause vascular damage in the form of an inflammatory reaction characterized by endothelial activation. Endothelial activation forms a pathological adaptation pattern so that it can induce the atherogenesis process. Several markers, such as E-selectin, platelet-derived micro particles (PMPs) and hematopoietic stem cell (HSC) can identify the activation of endothelial in circulating blood. Therefore, the deviation of vascular adaptation due to smoking can be detected early through the feedback mechanism between E-selectin, PMPs, and HSC.Purpose: This study aims to analyze the initial picture of the negative impact of smoking on vascular adaptation by measuring E-selectin, PMPs, and HSC in the peripheral blood circulation. Participant criteria and methods: Peripheral blood samples (5 mL) were taken from each participant, both the smoking group (n = 30) and the non-smoker group (n = 31) to obtain peripheral blood mononuclear cells (PBMNC). PBMNC was isolated using ficoll-based gradient centrifugation. The flow cytometry assay method used to measure the E-selectin, PMPs and hematopoietic stem cells.Results: The mean of circulating E-selectin in smokers was higher than that of non-smokers. On the other hand, the average number of PMPs and HSCs in smokers was lower than non-smokers.Conclusion: Smoking increases the risk of accelerated vascular block formation, as indicated by an increase in the amount of circulating E-selectin. The increase in E-selectin in the blood vessels mediates the increased adhesion of PMPs in the vascular area so that the number of circulating PMPs in smokers decreases. The decrease in circulating PMPs decreases the signal of vascular repair, which is characterized by a decline in the number of HSCs.Keywords: endothelial injury, cardiovascular disease, atherosclerosis, peripheral blood mononuclear cells, smoker

Background The pathomechanism of CVD is a complex and multifactorial process. The primary mechanism of CVD is atherosclerosis. Inflammation in atherogenesis raises the risk of hypoxia, which will activate hypoxia-inducible factor-1α (HIF1A). Also, together with lipoprotein-associated phospholipase A2 (Lp-PLA2), an inflammatory mediator for atherogenesis. Purpose This study aims to measure the hypoxia-inducible factor-1α (HIF1A) expression and its correlation to Lp-PLA2 expression at low-risk, intermediate, and high-risk CVD populations. Patients and Methods The study used a correlational analysis method with a total sampling technique in 160 individuals in the risk population. The atherosclerosis risk group was analyzed using the Framingham Risk Score and categorized into low, intermediate, and high-risk groups. Venous blood samples taken from respondents were measured using the ELISA method with Lp-PLA2 and HIF-1α as parameters. Data were analyzed using normality test, homogeneity test, one-way ANOVA, post hoc-Tukey HSD, and Pearson correlation. Results The concentration of HIF1A had a very strong correlation with Lp-PLA2 expression, both in the low-risk group (r = 0.512), intermediate (r = 0.512), and high (r = 0.715) (P

Background The pathomechanism of CVD is a complex and multifactorial process. The primary mechanism of CVD is atherosclerosis. Inflammation in atherogenesis raises the risk of hypoxia, which will activate hypoxia-inducible factor-1α (HIF1A). Also, together with lipoprotein-associated phospholipase A2 (Lp-PLA2), an inflammatory mediator for atherogenesis. Purpose This study aims to measure the hypoxia-inducible factor-1α (HIF1A) expression and its correlation to Lp-PLA2 expression at low-risk, intermediate, and high-risk CVD populations. Patients and Methods The study used a correlational analysis method with a total sampling technique in 160 individuals in the risk population. The atherosclerosis risk group was analyzed using the Framingham Risk Score and categorized into low, intermediate, and high-risk groups. Venous blood samples taken from respondents were measured using the ELISA method with Lp-PLA2 and HIF-1α as parameters. Data were analyzed using normality test, homogeneity test, one-way ANOVA, post hoc–Tukey HSD, and Pearson correlation. Results The concentration of HIF1A had a very strong correlation with Lp-PLA2 expression, both in the low-risk group (r = 0.512), intermediate (r = 0.512), and high (r = 0.715) (P