Resumo

Objective: S100B is a calcium binding protein that belongs to S100 protein family, produced and secreted by astrocytes in SNC. S100B have a neurotrophic or apoptotic effect depending on its concentration. It is well known that S100B is involved in several neuroinflammatory disorders, like Alzheimer’s disease. The aim of this study was to investigate the S100B protein secretion in primary astrocyte cultures exposed to steroid (dexametasone) and non-steroid (acetilsalicilic acid and diclofenac) anti-inflammatory compounds. Methods: Primary astrocyte cultures were prepared from cerebral cortex of newborn Wistar rats and were allowed to grow to confluence. S100B secretion was determined in culture medium by ELISA at 1 and 24 h of exposure to different anti-inflammatory compounds (dexametasone 0.1 µM, acetilsalicilic acid 100 µM and diclofenac 100 µM). Cell integrity and viability was evaluated by neutral red incorporation assay and LDH release. Results: Acetilsalicilic acid was able to reduce S100B secretion (67.1% ± 11.6, n = 7), while diclofenac and dexametasone increases S100B secretion in 1h of treatment (172.2% ± 13.8, n = 7 and 183.3% ± 23, n = 7, respectively). However, in 24 h of treatment, only dexametasone was able to induce a decrease in S100B secretion (43.8% ± 7.4, n = 7). No alteration in cell integrity and viability was observed. Conclusions: These results contribute to understanding the astroglial activity during neuroinflammation. The effect of different anti-inflammatory compounds in astrocytes, particularly on S100B secretion, reinforce the possibility of astrocytes became therapeutic target in neuroinflammatory diseases.