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Vitamin E Mempertahankan Kemampuan EPC yang Dipapar Glukosa Tinggi dalam Pelepasan NO dan Induksi Migrasi Sel Endotel (Vitamin E Protects the Ability of High Glucose Stimulated EPC's to Release NO and Induce Endothelial Cells Migration)
Role of EPCs on angiogenesis is impaired in diabetes. Study was design ed to investigate effect of vitamin E to ward ability of high glucose (HG) stimulated EPCs to release NO and inducemigration ofendothelial cells. Mononuclear cells were isolated from healthy subjects. After 7 days of culture, EPCs were cultured in 5 mM normal glucose in the absence or presence of 22 µM or 50 µM vitamin E, or cultured in 22 mM HG in the absence or presence of for 24 hours. EPCs function was assessed by evaluating HUVECs migration after administration of EPCs supematant that had previously been treated. HUVECs migration was evaluated using wound-healing migration assay. The levels of NO and H2O2 inEPCs supematant were measured by colorimetric assay. Superoxide of EPCs was evaluated by NBT assay. HG impaired EPCs ability to induce migration of HUVECs. Effect of HG could be reversed by co incubation with 50 µM vitamin E. Effect of vitamin E on ability ot EPCs was correlated with EPCs levels of NO, superoxide and H2O2. It can be concJuded that Vitamin E could maintain the ability of HG stimulated EPCs to release NO and induce migration of HUVECs through ROS-related mechanisms.
Keywords: EPCs, high qlucose, NO, ROS, vitamin E
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