Extracellular-Signal Regulated Kinase Signalling Pathway Mediates the Increased Proliferation of EPCs Treated with Garlic (Allium sativum) Extract, Purple Sweet Potato (Ipomoea batatas) Extract and Vitamin C

Yudi Her Oktaviono,Ferry Sandra,Alisia Yuana Putri,Yesita Rizky Firmansyah,Makhyan Jibril Al-Farabi

doi:10.5530/pj.2020.12.68

Abstract

The endothelial progenitor cell (EPCs) proliferation capability is reduced in the patient with stable coronary artery disease (SCAD). Garlic (Allium sativum), purple sweet potato (Ipomoea batatas), and vitamin C are proven antioxidant which potentially improve EPCs proliferation ability. Objective: To investigate the effect of garlic (Allium sativum), purple sweet potato (Ipomoea batatas), and vitamin C in EPCs proliferation from CAD patients and identify the involvement of Extracellular-Signal Regulated Kinase (ERK) Signalling Pathway. Material and Method: Mononuclear cells were isolated from SCAD patients and cultivated with colony-forming unit (CFU)-Hill medium and divided into untreated (control), garlic extract (10 mcg/ml and 100 mcg/ml), purple sweet potato extract (1 mcg/ml and 25 μg/ml), and vitamin C (10 μg/ml and 250 μg/ml). EPCs proliferation was measured using the MTT Assay. Results: This research shows that EPCs proliferation was increased in the treatment with garlic extract at 10 mcg/ml and 100 mcg/ml dose (0.267 ± 0,003 and 0.391 ± 0.008 ; p < 0.05), purple sweet potato extract at 1 mcg/ml and 25 μg/ml dose (0.250 ± 0.005 and 0.3562 ± 0.023 ; p < 0.001), and vitamin C at 10 μg/ml and 250 μg/ml dose (0.259 ± 0.016 and 0.306 ± 0.022 ; p < 0.001). Increased ERK expression was found in the treatment with garlic extract, purple sweet potato extract and vitamin C. Conclusion: Garlic extract, purple sweet potato extract, and vitamin C can increase EPC proliferation through the ERK signaling pathway.

Highlights

Coronary artery disease is a major health problem that causes mortality and reduction of life quality worldwide.[1]
It is suggested that oxidative stress play significant roles in Endothelial progenitor cells (EPCs) impairment through intracellular damage and balance disruption which will alter the control of apoptosis, proliferation, self-renewal, senescence, and differentiation of EPCs.[4,5,6]
Oxidative stress may disrupt the Extracellular-Signal Regulated Kinase (ERK) signaling pathway, which is important in EPCs proliferation.[2,7] the antioxidant is suggested to have a beneficial effect on impaired EPCs proliferation from patients with cardiovascular disease.[7,8]

Summary

Introduction

Coronary artery disease is a major health problem that causes mortality and reduction of life quality worldwide.[1] Endothelial progenitor cells (EPCs) from the patients with stable coronary artery disease (SCAD) had a progressive reduction of proliferation abilities, which worsen as the disease progressed[1]. Impaired EPCs proliferation will reduce vascular damage repair.[2] Lower EPCs proliferation in the patient with SCAD is associated with a higher incidence of cardiovascular events, mortality, and morbidity.[3]. Multiple pathways were suggested to be responsible for EPCs impairment in SCAD patients. It is suggested that oxidative stress play significant roles in EPCs impairment through intracellular damage and balance disruption which will alter the control of apoptosis, proliferation, self-renewal, senescence, and differentiation of EPCs.[4,5,6] Oxidative stress may disrupt the ERK signaling pathway, which is important in EPCs proliferation.[2,7] the antioxidant is suggested to have a beneficial effect on impaired EPCs proliferation from patients with cardiovascular disease.[7,8]

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Methods

Results

Conclusion