Fig. 4

LDclns induced glial activation and inflammatory factor production in A53T mice and WT mice. a Representative micrographs showed activation of GFAP positive astrocytes and Iba-1 positive microglia in SN of A53T mice and WT mice that had Ldclns. b Stereological counts of GFAP positive cells (genotype, F_(1,12) = 44.98, p < 0.0001; ligament, F_(1,12) = 29.69, p = 0.0001; interaction, F_(1,12) = 0.0173, p = 0.8974) and Iba-1 positive cells (genotype, F_(1,12) = 26.97, p = 0.0002; ligament, F_(1,12) = 44.94, p < 0.0001; interaction, F_(1,12) = 0.5831, p = 0.4599) in SN of A53T-LDclns mice. c Percentage of positive area for GFAP (genotype, F_(1,12) = 18.54, p = 0.0010; ligament, F_(1,12) = 21.86, p = 0.0005; interaction, F_(1,12) = 0.0012, p = 0.9732) and Iba-1 (genotype, F_(1,12) = 36.02, p < 0.0001; ligament, F_(1,12) = 63.02, p < 0.0001; interaction, F_(1,12) = 0.5401, p = 0.4765) in SN. d-g Representative immunoblotting bands and densitometry analysis of IL-1β, IL-6 and TNF-α of ventral midbrain samples. Levels of IL-1β (genotype, F_(1,8) = 49.97, p = 0.0001; ligament, F_(1,8) = 27.86, p = 0.0007; interaction, F_(1,8) = 0.2273, p = 0.6463), IL-6 (genotype, F_(1,8) = 47.23, p = 0.0001; ligament, F_(1,8) = 36.64, p = 0.0003; interaction, F_(1,8) = 2.186, p = 0.1776) and TNF-α (genotype, F_(1,8) = 28.19, p = 0.0007; ligament, F_(1,8) = 48.21, p = 0.0001; interaction, F_(1,8) = 0.2262, p = 0.6471) were increased in both A53T mice and WT mice after LDclns. Data represent mean ± SEM from 3 to 4 mice per group; data in e-g are from two independent experiments