Fig. 7. GlcN and Thiamet G promote anti-inflammatory microglial polarization in the SN of LPS-induced PD model mice.

LPS (5 μg) was stereotaxically injected into the SN of mouse brains to induce neuroinflammation. GlcN (200 mg/kg) and Thiamet G (ThiaG; 20 mg/kg) were administered intraperitoneally three times per week for four weeks. A, D Western blot analyses of SN tissue lysates were performed to evaluate microglial polarization markers, including TLR4, CD86, CD68 (M1 markers), and CD163, Arg1 (M2 markers). β-actin was used as a loading control. Protein expression levels were quantified and normalized to β-actin (n = 3/group). B, E Phosphorylation levels of STAT3 and ERK were assessed using phospho-specific and total antibodies. The ratios of p-STAT3/STAT3 and p-ERK/ERK were calculated and normalized accordingly (n = 3/group). C, F PPARγ and p-CREB/CREB levels were evaluated by immunoblotting. Densitometric analyses were performed with normalization to β-actin or total CREB (n = 3/group). G, I Representative immunofluorescence images of CD163 (red), TH (green), and DAPI (blue) in the SN region to visualize anti-inflammatory (M2) microglial phenotypes. Scale bar: 50 μm (n = 3/group). H, J Representative immunofluorescence images of CD86 (red), TH (green), and DAPI (blue) in the SN region to visualize pro-inflammatory (M1) microglial phenotypes. 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.