Fig. 5

Sevo reduces HES1 expression by activating FGF2/EZH2 axis to suppress neurological injury in TBI rats. Sevo-treated TBI rats were treated with sh NC + oe NC, sh NC + oe EZH2, sh FGF2 + oe NC, or sh FGF2 + oe EZH2. A Neurological function assessment by mNSS, brain water content evaluation and motor function score in TBI rats. B RT-qPCR and Western blot analysis detection of HES1 expression in the cortical tissue of TBI rats. C Immunofluorescence staining analysis of HES1 expression in the cortical tissue of TBI rats (scale bar: 25 μm). D RT-qPCR and Western blot analysis detection of BDNF expression in the cortical tissue of TBI rats. E RT-qPCR and Western blot analysis of NeuN expression in the cortical tissue of TBI rats. F Neuronal damage assessed by Nissl staining. G TUNEL-positive cells in the cortical tissue of TBI rats. H Protein expression of autophagy-related genes (LC3-I, LC3-II, Beclin-1, and P62) in the cortical tissue of TBI rats detected by Western blot analysis. TBI hippocampal neurons were treated with sh NC + oe NC, sh NC + oe EZH2, sh FGF2 + oe NC, or sh FGF2 + oe EZH2. I Neuronal damage assessed by cell immunofluorescence staining. J The apoptosis of hippocampal neurons measured by flow cytometry. In panel A–H, n = 12 for rats upon each treatment. *p < 0.05 vs. Sevo-treated TBI rats or hippocampal neurons treated with sh NC + oe NC. ^#p < 0.05 vs. Sevo-treated TBI rats or hippocampal neurons treated with sh NC + oe EZH2. Cell experiments were conducted three times independently