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- W2904404809 abstract "Developmental exposure to ethanol may cause fetal alcohol spectrum disorders (FASD), and the immature central nervous system (CNS) is particularly vulnerable to ethanol. In addition to vulnerability in the developing brain, we previously showed that ethanol also caused neuroapoptosis, microglial activation, and neuroinflammation in the spinal cord. Minocycline is an antibiotic that inhibits microglial activation and alleviates neuroinflammation. We sought to determine whether minocycline could protect spinal cord neurons against ethanol-induced damage. In this study, we showed that minocycline significantly inhibited ethanol-induced caspase-3 activation, microglial activation, and the expression of pro-inflammatory cytokines in the developing spinal cord. Moreover, minocycline blocked ethanol-induced activation of glycogen synthase kinase 3 beta (GSK3β), a key regulator of microglial activation. Meanwhile, minocycline significantly restored ethanol-induced inhibition of protein kinase B (AKT), mammalian target of the rapamycin (mTOR), and ERK1/2 signaling pathways, which were important pro-survival signaling pathways for neurons. Together, minocycline may attenuate ethanol-induced damage to the developing spinal cord by inhibiting microglial activation/neuroinflammation and by restoring the pro-survival signaling." @default.
- W2904404809 created "2018-12-22" @default.
- W2904404809 creator A5001598173 @default.
- W2904404809 creator A5006822602 @default.
- W2904404809 creator A5031625792 @default.
- W2904404809 creator A5041424398 @default.
- W2904404809 creator A5058262905 @default.
- W2904404809 date "2019-09-01" @default.
- W2904404809 modified "2023-10-17" @default.
- W2904404809 title "Minocycline attenuates ethanol-induced cell death and microglial activation in the developing spinal cord" @default.
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