Fig 2: BSYS promotes oligodendrocyte maturation in vitro by ameliorating the neurotoxic impacts of A1 astrocytes. (a) MDA content, (b) SOD level, and (c) GSH-Px activity of OLN-93 cells were determined utilizing the respective commercial kit. (d) The expression of PLP in OLN-93 cells was determined by immunocytofluorescence staining. Scale bars: 50 μm. (e) The relative protein expression level of MOG, PLP, MBP, and CNPase in astrocytes is shown using illustrative blots and statistical graphs. Data are reported as means ± SD; contrasted to the ASC group, ∗∗P < 0.01, ∗∗∗P < 0.001; contrasted with the ASC+BSYS group, △△△P < 0.001; contrasted to the ASC+BSYS+miR-NC group, ▲P < 0.05, ▲▲P < 0.01, and ▲▲▲P < 0.001.

Fig 3: DEHP-induced impairment of oligodendrocyte homeostasis, tau hyperphosphorylation, and loss of synaptic integrity in the hippocampus of adult female rats. (A,B) Representative immunofluorescence (IF) images and quantification of oligodendrocyte lineage markers (Olig1, Olig2, PLP1) and phosphorylated tau (p-tau231, p-tau396). (C,D) Representative IF staining and quantitative analysis of pre-synaptic (VAMP2, Syntaxin) and post-synaptic/dendritic proteins (SAP102, MAP2, CaMKIIα, SPN). (E) Representative Western blot bands for Olig1, synaptic proteins, and tau phosphorylation markers. GAPDH or α-tubulin was used as a loading control. (F) Quantification of relative protein levels normalized to GAPDH or α-tubulin. (Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. Ctrl; n.s., not significant. n = 3).