Fig. 1

LRRK2 kinase inhibition attenuates inflammation in BV2 cells. a BV2 cell lysates treated with LPS, LPS and IN-1, and IN-1 alone or DMSO as control were subjected to immunoblotting using COX-2 and IL-1β antibodies. b Quantification of COX-2 and IL-1β are normalized for α-actin protein. Data are representative of three independent experiments (bars represent the mean ± SEM; one-way ANOVA comparing all groups, Tukey’s multiple comparison post hoc test; ***p < 0.001). c BV2 cell lysates treated with LPS, LPS and GSK, and GSK alone or DMSO as control were subjected to immunoblotting using COX-2 and IL-1β antibodies. d Quantification of COX-2 and IL-1β are normalized for β-tubulin. Data are representative of three independent experiments (bars represent the mean ± SEM; one-way ANOVA comparing all groups, Tukey’s multiple comparison post hoc test; **p < 0.01 and ***p < 0.001). e BV2 cell lysates treated with LPS, LPS and GSK, and GSK alone or DMSO as control were subjected to semi-quantitative PCRs. f Quantification of COX-2 and IL-1β mRNAs are normalized for GAPDH. Data are representative of three independent experiments (bars represent the mean ± SEM; one-way ANOVA comparing all groups, Tukey’s multiple comparison post hoc test; *p < 0.05, **p < 0.01 and ***p < 0.001). g BV2 cell lysates treated with LPS and DMSO as control were subjected to immunoblotting using LRRK2 and β-tubulin antibodies. h Quantification of LRRK2 protein is normalized for β-tubulin. Data are representative of six independent experiments (bars represent the mean ± SEM; unpaired t test)