Abstract

Endothelial Progenitor Cells (EPCs) have an important role in endothelial dysfunction repairment through neovasculogenesis and cardiac myocytes regeneration. However, EPCs migration is greatly reduced in the patient with Coronary Artery Disease (CAD). Allicin and Vitamin C are hypothesized to improve EPCs migration due to its antioxidant properties. Objective: To investigate the effect of Allicin and its combination with Vitamin C in EPCs migration of CAD patients. Material and Method: Mononuclear cells were isolated from CAD patients and cultured on fibronectin-coated plates with colony-forming unit Hill medium. The cells were divided into untreated (control), Allicin treatment (dose 100 mcg/ml, 200 mcg/ml, 400 mcg/ ml), and each dose of Allicin combined with 250 mcg/mL of Vitamin C. EPCs migration was assessed with Transwell Migration Assay Kit and evaluated by using statistical tests. Results: This research shows that EPC migration was significantly higher in the treatment. Allicin at all dose (dose 100 mcg/ml, 200 mcg/ml, 400 mcg/ml) and its combination with 250 mcg/mL of vitamin C compared to untreated group (p<0.05). Allicin increase EPCs migration in a dosedependent manner. However, the only combination of 400 mcg/ml Allicin with 250 mcg/mL of vitamin C which has significantly higher EPCs migration compared to Allicin treatment alone. Conclusion: Allicin improves EPCs migration in a dose-dependent manner. Improvement of the migration only observed on the Allicin dose 400 mcg/ml with Vitamin C.

Highlights

  • Coronary Artery Disease is the leading cause of cardiovascular death worldwide and responsible for 17.3 million deaths in 2013.1,2 In 2030, it is projected that CAD in the United States reached 49,3%.3 In Indonesia, the Ministry of Health confirmed that CAD caused 12,9% of deaths from non-communicable disease.[4]

  • The cells were divided into untreated, Allicin treatment, and each dose of Allicin combined with 250 mcg/mL of Vitamin C

  • Endothelial Progenitor Cells (EPCs) migration was improved in a dose-dependent manner on the treatment with Allicin

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Summary

Introduction

Coronary Artery Disease is the leading cause of cardiovascular death worldwide and responsible for 17.3 million deaths in 2013.1,2 In 2030, it is projected that CAD in the United States reached 49,3%.3 In Indonesia, the Ministry of Health confirmed that CAD caused 12,9% of deaths from non-communicable disease.[4]. Coronary Artery Disease is the leading cause of cardiovascular death worldwide and responsible for 17.3 million deaths in 2013.1,2 In 2030, it is projected that CAD in the United States reached 49,3%.3. In Indonesia, the Ministry of Health confirmed that CAD caused 12,9% of deaths from non-communicable disease.[4] Early-stage of CAD is marked by endothelial injury which could progress to atherosclerosis.[5] Endothelial injury repair requires colonization of EPCs derived from blood marrow-derived progenitor cells.[6] Previous studies have shown the benefit of EPCs to repair damaged endothelial by differentiation into the mature endothelial cell to induce vasculogenesis. Emerging evidence showed that the decrease of EPCs number in patients with CAD is related to the long term exposure to pro-inflammatory cytokines and oxidative stress.[10]

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