ELIGLUSTAT, AN INHIBITOR OF GB3 RECEPTOR SYNTHESIS, PROTECTS HUMAN MICROVASCULAR ENDOTHELIAL CELLS FROM SHIGA TOXIN TYPE 2 CYTOTOXICITY.

GOMEZ FERNANDO; VELEZ GUTIERREZ DANIEL; BALESTRACCI ALEJANDRO; IBARRA CRISTINA; AMARAL MARÍA M

Mar del Plata

Congreso; Reunión Anual SAIC ? SAFE ? SAB ? SAP 2019; 2019

SAIC SAFE SAB SAP

Hemolytic Uremic Syndrome associated toShiga toxin (Stx)-producing E. coli infection is the most commoncause of acute renal failure (ARF) in children in Argentina. Stx2binds the globotriaosylceramide (Gb3) receptor and causes directdamages on human renal microvascular endothelial cells (HGEC).In this work, we assayed the action of a Gb3 synthesis inhibitor,Eliglustat (EG), to prevent the Stx2 cytotoxicity on human renalcells. Cell viability was analyzed by neutral red uptake and dataare expressed as mean ± SEM. Cell morphology analysis wasevaluated by light microscopy after staining with H&E. Cellcounts were performed on five fields and cell area values wereobtained using Image J software. Necrosis and apoptosis weredetected by flow cytometry after Annexin V-FITC/PI doublestaining assay. Non-cytotoxic concentrations of EG wereestablished on HGEC treated with EG (0.05 ? 50 µM) for 120 h.While EG (50 µM) caused a significant decreased of cell viability(8.3 ± 0.9% vs. Ctrl: 100 ± 2.7 %, n= 3, p