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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: The neuroprotective mechanism of sevoflurane in rats with traumatic brain injury via FGF2

Fig. 2

Sevo activates FGF2 to relieve neurological deficits and neuronal death in TBI rats. A Differential analysis of the GSE141242 dataset related to Sevo-treated rat brain tissues. B The expression heat map of the top 15 DEGs with the smallest p-value. C Intersection of the top 15 DEGs with the smallest p-value with TBI-related genes obtained through GeneCards database. D FGF2 expression in TBI rats after Sevo treatment analyzed by gene microarray data. E Western blot analysis of FGF2 expression in the cortical tissue of sham-operated, TBI, or Sevo-treated TBI rats. Sevo-treated TBI rats were treated with sh NC, sh FGF2, oe NC, or oe FGF2. F Immunofluorescence analysis of FGF2 expression in the cortical tissue of TBI rats (scale bar: 25 μm). G Western blot analysis of FGF2 expression in the cortical tissue of TBI rats. H Neurological function evaluation by mNSS, brain water content measurement and motor function score in TBI rats. I The expression of BDNF determined by Western blot analysis and RT-qPCR in the cortical tissue of TBI rats. J RT-qPCR detection and Western blot analysis of the expression of NeuN in the cortical tissue of TBI rats. K Nissl staining of the hippocampal neuronal damage in the cortical tissue of TBI rats. L TUNEL-positive cells in the cortical tissue of TBI rats. M Western blot analysis of protein expression of autophagy-related genes (LC3-I, LC3-II, Beclin-1, and P62) in the cortical tissue of TBI rats. TBI hippocampal neurons were treated with oe NC, sh NC, oe FGF2 or sh FGF2. N Neuronal damage assessed by cell immunofluorescence assay. O Axonal length measurement of hippocampal neurons (After primary hippocampal neurons were cultured for 48 h, Tau-1 was used to specifically identify axons, with red fluorescent markers in the figure; MAP2 was used to specifically identify dendrites, with green fluorescent markers, with a scale of 25 μm). P The apoptosis of hippocampal neurons measured by flow cytometry. In panel EM, n = 12 for rats upon each treatment. *p < 0.05 vs. sham-operated rats, Sevo-treated TBI rats or hippocampal neurons treated with oe NC; #p < 0.05 vs. TBI rats, Sevo-treated TBI rats or hippocampal neurons treated with sh NC. Cell experiments were conducted three times independently

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