AI Summary & Key Takeaways
AI InsightMoreover, M administration reversedthe neuronal loss observed in DG during SE.CONCLUSION: These results suggest that serum S100B is a candidate biomarker for monitoring neuroinflammation and that it mayalso help predict diagnosis and prognosis.
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Özet
AIM: To investigate possible correlations between serum S100B levels and microglial/astrocytic activation in status epilepticus (SE)in lithium–pilocarpine-exposed rat hippocampi and whether serum S100B levels linearly reflect neuroinflammation. Additionally, toassess the effects of minocycline (M), an inhibitor of neuroinflammation.MATERIAL and METHODS: Rats were divided into 4 groups (6/group), namely, control (C), sham, SE, and SE+M. Animals wereexposed to lithium–pilocarpine to induce SE in the SE and SE+M groups. Cardiac blood was collected to measure S100B levels,and coronal brain sections including the hippocampus were prepared to examine microglial/astrocytic activation and to evaluateneuroinflammation at day 7 of SE.RESULTS: Serum S100B levels, OX42 (+) microglia in CA1, and GFAP (+) astrocytes in both CA1 and dentate gyrus (DG) werehigher in the SE+M group than in the C group. Most importantly, highly positive correlations were found between S100B levelsand microglial activation in CA1, apart from astrocytic activation in CA1 and DG. Unexpectedly, microglial activation in CA1 andastrocytic activation in DG were also enhanced in the SE+M group compared with the C group. Moreover, M administration reversedthe neuronal loss observed in DG during SE.CONCLUSION: These results suggest that serum S100B is a candidate biomarker for monitoring neuroinflammation and that it mayalso help predict diagnosis and prognosis.