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. 2026 Mar 28;12:121. doi: 10.1038/s41531-026-01319-6

Fig. 6. GlcN and Thiamet G enhance M2 polarization and suppress M1 signaling in microglia.

Fig. 6

Primary microglial cells were stimulated with LPS (400 ng/mL) for 24 h in the presence or absence of GlcN (5 mM) or Thiamet G (ThiaG; 1 μM) to assess phenotypic polarization and relevant signaling mechanisms. A, D Western blot analysis was performed to assess the expression of microglial polarization markers, including TLR4, CD86, CD68 (M1 markers), and CD163, Arg1 (M2 markers). β-actin was used as a loading control. Protein levels were quantified and normalized to β-actin (n = 3/group). B, E Expression of phosphorylated STAT3 (p-STAT3) and phosphorylated ERK (p-ERK) was analyzed along with their respective total protein levels. p-STAT3 and p-ERK expression was normalized to total STAT3 and ERK, respectively (n = 3/group). C, F Expression of PPARγ and phosphorylated CREB (p-CREB) was evaluated by western blot. p-CREB levels were normalized to total CREB, and PPARγ levels were normalized to β-actin (n = 3/group). G Representative immunofluorescence images of CD86 (red), Iba1 (green), and DAPI (blue) in primary microglial cells. Scale bar: 50 μm (n = 3/group). H Representative immunofluorescence images of Arg1 (red), Iba1 (green), and DAPI (blue) in primary microglial cells. Scale bar: 50 μm (n = 3/group). Data are presented as mean SEM; *p < 0.05, **p < 0.01, ***p < 0.001 versus control, #p < 0.05, ##p < 0.01, ###p < 0.001 versus LPS. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc multiple comparison test.