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. 2021 Oct 12;7:289. doi: 10.1038/s41420-021-00676-w

Fig. 4. Accumulation of p-α-syn in SCs probably mediated by TLR2 through TLR2/NF-κB pathway.

Fig. 4

As a TLR2 inhibitor, CU-CPT22 was used to block TLR2/NF-κB pathway. A Level of p-α-syn was remarkably increased after MPTP exposure (20 mg/kg) and moderately elevated after CU-CPT22 + MPTP treatment (3 mg/kg; 20 mg/kg), while t-α-syn had no obvious changes. B Compared to saline group, the expression of TLR2 was higher in sciatic nerves for MPTP group and mildly upregulated in CU-CPT22 + MPTP group. C MyD88 in sciatic nerves of MPTP group was elevated than saline group, and level in CUCPT22 + MPTP group displayed a decrease compared with MPTP group. D The expression of p-NF-κB was higher in sciatic nerves of MPTP group than saline group, with a reduction in CUCPT22 + MPTP group compared to MPTP group. The β-actin was used as housekeeping and data were normalized to β-actin expression. Data were presented as mean ± SEM and analyzed by one-way ANOVA followed by Tukey’s post hoc test; n = 6. *p < 0.05, **p < 0.01 vs. saline group; #p < 0.05, ##p < 0.01 vs. MPTP group. p-α-syn: phosphorylated α-synuclein; SCs: Schwann cells; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; t-α-syn: total α-synuclein; TLR: toll-like-receptor; MyD88: myeloid differentiation-factor 88; NF-κB: nuclear factor kappa-B; p-NF-κB: phospho-NF-κB; SEM: standard error of the mean; ANOVA: analysis of variance.