Background Oxygen-glucose deprivation (OGD) is a widely used in vitro model for ischemic brain injury, which leads to cell death. Prevention and attenuation of brain injury by the tetracycline-antibiotic minocycline has been largely attributed to suppression of microglial activation.
Methods Using mono-cultures of rat oligodendroglial precursor cells (OPC) exposed to oxygen-glucose deprivation (OGD), we investigated direct effects of minocycline on survival, proliferation, and maturation of oligodendroglial lineage cells.
Results OGD for 2 h decreased the number of A2B5+ cells and the amount of proliferating Ki67+ A2B5+ cells by 50% which was both attenuated by minocycline in a dose-dependent fashion. The reduced numbers of O4+ cells at 72 h and of O1+ cells at 120 h after OGD were partially restored by minocycline. In OPC, OGD caused an increase of reactive oxygen species (ROS) production and of TUNEL-positive cell numbers which was abolished by minocycline, possibly via induction of superoxide dismutase. Minocycline also prevented OGD-induced downregulation of the expression of the transcription factors Sox10 and Olig2, and of the maturation markers 2’3’ cyclic nucleotide phosphodiesterase (CNP) and myelin basic protein (MBP).
Conclusion The results demonstate that minocycline exerts direct protective actions on oligodendroglial lineage cells.
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