Fig. 9: In vivo models verified that KDM2B regulates ferroptosis through OGT O-GlcNAcylation pathway to affect neuronal injury.

KDM2B knockdown MCAO mice were constructed and treated with OSMI-1. The mice were divided into the MCAO group, MCAO + sh-KDM2B group, and MCAO + sh-KDM2B + OSMI-1 group. A Statistical analysis of cerebral infarct size in different groups, n = 6. B Nerve injury scores in different groups, n = 6. C Statistics of hydrocephalus in different groups, n = 6. D The brain tissues of different groups were stained with HE and Nissl staining, and the protein expression of OGT in different groups was detected by immunohistochemistry. Scale bar: 100 μm. E The protein expression levels of NeuN and PSD95 in different groups were detected by WB, n = 6. F Open field‑testing and rotarod test in different groups of mice, n = 10. H The contents of THF-α and IL-10 in different groups were determined, n = 3. G GSH and ROS contents were measured in different groups, n = 3. I The mechanism roadmap. Results were expressed as group mean ± standard deviation. *p < 0.05 vs. MCAO group; #p < 0.05 vs. MCAO + Sh-KDM2B group.