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Bioactive glasses (BGs), also known as bioglasses, are very attractive and versatile materials that are increasingly being used in dentistry. For this study, two new bioglasses-one with boron (BG1) and another with boron and vanadium (BG2)-were synthesized, characterized, and tested on human dysplastic keratinocytes. The in vitro biological properties were evaluated through pH and zeta potential measurement, weight loss, Ca2+ ions released after immersion in phosphate-buffered saline (PBS), and scanning electron microscopy (SEM) coupled with energy dispersive spectroscopy (EDS) analysis. Furthermore, biocompatibility was evaluated through quantification of lactate dehydrogenase activity, oxidative stress, transcription factors, and DNA lesions. The results indicate that both BGs presented the same behavior in simulated fluids, characterized by high degradation, fast release of calcium and boron in the environment (especially from BG1), and increased pH and zeta potential. Both BGs reacted with the fluid, particularly BG2, with irregular deposits covering the glass surface. In vitro studies demonstrated that normal doses of the BGs were not cytotoxic to DOK, while high doses reduced cell viability. Both BGs induced oxidative stress and cell membrane damage and enhanced NFkB activation, especially BG1. The BGs down-regulated the expression of NFkB and diminished the DNA damage, suggesting the protective effects of the BGs on cell death and efficacy of DNA repair mechanisms.
RESUMEN
INTRODUCTION: Exposure of the endothelial cells to hypoxia, the decrease in oxygen supply can trigger an endothelial response. This response is involved in inflammatory diseases, tumorigenesis, and also with the micro vascular damage associated with aging. The aim of our study was to determine the hypoxia/re-oxygenation induced response in vitro, using human umbilical vein endothelial cells (HUVEC) cultures, at different time points with focus on cell viability, apoptosis oxidative stress and angiogenesis stimulation. MATERIALS AND METHODS: Cells were exposed to 10%, 5% or 0% O2 for 6h, 12h, and 24h. Viability was measured through colorimetry, apoptosis - annexin V-FITC staining, DNA lesions (γH2AX), endothelial activation (sICAM1), angiogenesis (HIF1α), oxidative stress (malondialdehyde, superoxidismutase and NFκB activation) were determined by ELISA, Western Blot and spectrophotometry. RESULTS AND DISCUSSION: Hypoxia decreased viability, increased apoptosis, oxidative stress, endothelial activation and angiogenesis, depending on O2 concentration and time exposure. Short exposures to 5% and 10% O2, efficiently activated anti-apoptotic mechanisms through NFκB activation, HIF1α and γH2AX related DNA damage repair pathways. However, severe hypoxia and longer exposures to mild hypoxia induced high oxidative stress related damage and eventually led to apoptosis, through strong increases of HIF1α and accumulating DNA lesions.