Fig. 3

Effects of silencing Fgf2 on neuronal apoptosis, oxidative stress injury, and neuroinflammation in the in vitro sevoflurane model. Note: (A) RT-qPCR analysis of Fgf2 mRNA expression in sevoflurane model neurons; (B) Western blot analysis of Fgf2 protein expression in sevoflurane model neurons; (C) Flow cytometry analysis of apoptosis in primary cortical neurons from different groups (Q2 and Q3 quadrants); (D) Statistical analysis of the percentage of apoptosis in different groups of primary cortical neurons (Q2 and Q3 quadrants); (E–F) Generation of reactive oxygen species (ROS) in different groups of primary cortical neurons (green fluorescence represents ROS activity marker, scale bar = 50 μm); (G) Measurement of malondialdehyde (MDA) content in different groups of primary cortical neurons using the TBARS assay; (H) Measurement of glutathione (GSH) content in different groups of primary cortical neurons using the glutathione assay kit; (I–K) RT-qPCR analysis of TNF-α, IL-6, and IL-1β expression in different groups of primary cortical neurons. ** represents a difference compared to the Control group or Sevo + sh-NC group (P < 0.01), ^## represents a difference compared to the Sevo + sh-Fgf2 group (P < 0.01), and the cell experiments were repeated 3 times