Author/Authors :
-، - نويسنده Medical Research Center, Faculty of Medicine, Maranatha Christian University, Jl. Prof. Drg. Suria Sumantri 65, Bandung 40164, West Java, Indonesia Widowati, Wahyu , -، - نويسنده Biomolecular and Biomedical Research Center, Aretha Medika Utama, Jl. Babakan Jeruk 2 no 9, Bandung, 40163, West Java, Indonesia Widyanto, Rahma Micho , -، - نويسنده Medical Research Center, Faculty of Medicine, Maranatha Christian University, Jl. Prof. Drg. Suria Sumantri 65, Bandung 40164, West Java, Indonesia Husin, Winsa , -، - نويسنده Medical Research Center, Faculty of Medicine, Maranatha Christian University, Jl. Prof. Drg. Suria Sumantri 65, Bandung 40164, West Java, Indonesia Ratnawati, Hana , -، - نويسنده Faculty of Pharmacy, Pancasila University, Jl Jagakarsa, Jakarta, Indonesia Laksmitawati, Dian Ratih , -، - نويسنده Department of Medical Chemistry and Biochemistry, Faculty of Medicine, Lambung Mangkurat University, Banjarmasin, South Kalimantan, Indonesia Setiawan, Bambang , -، - نويسنده Department of Pharmacology, Faculty of Medicine, Brawijaya University, Jl. Veteran, Malang, 65145, East Java, Indonesia Nugrahenny, Dian , -، - نويسنده Stem Cell and Cancer Institute, JL. A. Yani no.2 Pulo Mas, Jakarta, 13210, Indonesia Bachtiar, Indra
Abstract :
Objective(s):Many studies have reported that tea consumption decreases cardiovascular risk, but the mechanisms remain unclear. Green tea is known to have potent antioxidant and free radical scavengingactivities. This study aimed to investigate whether green tea extract (GTE) can protect endothelial progenitors cells (EPCs) against oxidative stress through antioxidant mechanisms. Materials and Methods: Mononuclear cells (MNCs) were isolated from peripheral blood by density gradient centrifugation with Ficoll. The cells were then plated on fibronectin-coated culture dishes. After 7 days of culture, EPCs were characterized as adherent cells double positive for DiI-ac-LDL uptake and lectin binding. EPCs were further identified by assessing the expression of CD34/45, CD133, and KDR. EPCs were then treated with hydrogen peroxide (H2O2) at doses of 50, 100, 200 µM and incubated with or without GTE (25 µg/ml). The intracellular reactive oxygen species (ROS) levels were detected by flow cytometry using a 2’,7’-dichlorofluorescein diacetate (DCF-DA) fluorescentprobe. Results: GTE ameliorated the cell viability of EPCs induced by H2O2 at doses of 50, 100, 200 µM for about 25.47, 22.52, and 11.96% higher than controls, respectively. GTE also decreased the intracellular ROS levels of EPCs induced by H2O2 at doses of 50, 100, 200 µM for about 84.24, 92.27, and 93.72% compared to controls, respectively. Conclusion: GTE improves cell viability by reducing the intracellular ROS accumulation in H2O2-induced EPCs.
