Resumo

Objectives: Inflammatory response in brain is associated with neurodegenerative disorders, like Alzheimer’s disease. S100B is a calcium-binding protein secreted by astrocytes and elevated levels of this protein have been observed in neurodegenerative diseases. Lipopolysaccharide (LPS) is widely used in models of neuroinflammation. However, there are not studies showing the effect of LPS in the secretion of S100B. The aim of this study was to investigate the influence of LPS exposure in acute hippocampal slices on S100B secretion and glutathione (GSH) content. Methods: Hippocampi of Wistar rats were dissected and cut into 0.3 mm slices, which were stabilized in HEPES-buffered saline for 2 h. LPS was added at 0.1, 1.0 and 10 µg/mL for 1 h. S100B measurement was carried out by ELISA and GSH content was carried out by a fluorimetric assay. Cell viability was measured by neutral red and MTT assays. Results: LPS at 0.1 µg/mL and 1 µg/mL was able induced a decrease in S100B secretion in 1 h of exposure (0.456 ng/mL ± 0.090, n = 5 and 0.374 ng/mL ± 0.095, n = 5, respectively) in relation to basal levels (0.795 ng/mL ± 0.139, n = 5), but conversely, LPS at 10 µg/mL increased S100B secretion (1.164 ng/mL ± 0.081, n = 7). No change in cell viability was observed with neutral red incorporation or MTT reduction assays. Moreover, in all these concentrations LPS caused a decrease (about 40%) in the levels of GSH. Conclusions: Our data suggest that LPS affect astroglial activity modulating the secretion of S100B, a neurotrophic cytokine, and the content of GSH, an important component of antioxidant defense.