Fig. 1
NLRP3 deficiency attenuates motor dysfunctions and dopaminergic neuronal loss in MPTP-treated mice. a–c Nlrp3+/+ or Nlrp3−/− mice were administered with PBS or MPTP (40 mg/kg) for 5 days and then examined for motor activity impairment as described in the Methods. a The latent time to hold the bar in the string test 24 h post the final PBS or MPTP administration (Nlrp3+/+ mice, PBS (n = 6), MPTP (n = 10); Nlrp3−/− mice, PBS (n = 6), MPTP (n = 11)). b The latent time to hold the bar in the catalepsy test 1 h post the final PBS or MPTP administration. (PBS (n = 6), MPTP (n = 11)). c The severity of hindlimb clasping in PBS- (n = 6) or MPTP-treated (n = 11) mice 1 h post the final PBS or MPTP administration. d Representative immunofluorescence image of the fixed brain sections containing SN of PBS- or MPTP-treated Nlrp3+/+ or Nlrp3−/− mice after staining with anti-TH antibody (green). DAPI represents the nuclear signal (blue). Scale bars, 200 μm. e Quantification of relative TH-positive cells per DAPI in confocal images of PBS- or MPTP-treated Nlrp3 +/+ or Nlrp3−/− mice (n = 4). f Quantification of striatal dopamine levels of PBS- or MPTP-treated Nlrp3+/+ or Nlrp3−/− mice as determined by HPLC-MS/MS (Nlrp3+/+ mice, PBS (n = 11), MPTP (n = 11); Nlrp3−/− mice, PBS (n = 11), MPTP (n = 10)). Data were expressed as the mean ± SEM. Asterisks indicate significant differences (*P < 0.05, **P < 0.01, ***P < 0.001)
