Abstract
Impairment of the endothelial progenitor cells (EPCs) ability to proliferate and migrate in the patients with coronary heart disease (CHD) is partly caused by oxidative stress. This research evaluates the effect of treatment with Ipomoea batatas L./purple sweet potato (PSP) extract and l-ascorbic acid on the proliferation and migration of impaired EPCs. EPCs were isolated from CHD patient’s peripheral blood. EPCs culture were cultivated and divided into control (untreated), PSP extract treatment (dose 1 and 25 μg/mL), and l-ascorbic acid treatment (dose 10 and 250 μg/mL) groups for 48 h. EPCs proliferation was analyzed with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation assay, and migration was evaluated with the cell migration assay kit. Statistical tests were evaluated using SPSS 25.0. This research showed that EPCs proliferation and migration was significantly higher in all PSP extract and l-ascorbic acid treatment compared to the control (p < 0.001). EPCs migration on treatment with a PSP extract dose of 25 μg/mL was significantly higher compared to the treatment with l-ascorbic acid dose of 250 μg/mL (303,000 ± 1000 compared to 215,000 ± 3000 cells, p< 0.001). In conclusion, both treatments with PSP extract and l-ascorbic acid can improve the proliferation and migration of impaired EPCs. At the dose of 25 μg/mL, PSP extract seems to be superior to the l-ascorbic acid dose of 250 μg/mL to improve EPCs migration.
Highlights
Coronary heart disease (CHD) is responsible for around 33% of death in individuals aged 35 and over in the World [1,2,3]
Endothelial progenitor cells (EPCs) from the patients with CHD had reduced proliferation, and migration abilities, which can be worse as the disease progressed [5]
Patients with low EPCs count and impaired migration activity have a higher incidence of cardiovascular events, mortality, and morbidity compared to patients with higher total EPCs and normal migration capabilities [7]
Summary
Coronary heart disease (CHD) is responsible for around 33% of death in individuals aged 35 and over in the World [1,2,3]. In Indonesia, the Ministry of Health reported that 12.9% of the mortality was caused by CHD [4]. Endothelial progenitor cells (EPCs) from the patients with CHD had reduced proliferation, and migration abilities, which can be worse as the disease progressed [5]. Impaired EPCs proliferation and migration capabilities can reduce its ability to repair vascular damage [5,6]. Patients with low EPCs count and impaired migration activity have a higher incidence of cardiovascular events, mortality, and morbidity compared to patients with higher total EPCs and normal migration capabilities [7]. Multiple pathways were suggested to be responsible for EPCs impairment in CHD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
