Research Paper Volume 12, Issue 23 pp 23619—23646

Pathomechanism characterization and potential therapeutics identification for SCA3 targeting neuroinflammation


Figure 5.

Effects of the tested compounds on IL-1β- and TNF-α-mediated pathways in inflamed ATXN3/Q75-GFP SH-SY5Y cells. Retinoic acid (10 μM)-differentiated ATXN3/Q75-GFP SH-SY5Y cells were treated with the tested compound (10 μM) for 8 h, followed by inducing ATXN3/Q75 expression for 6 days, with retinoic acid removal and HMC3 conditioned medium addition (CM/+IFN-γ or CM/–IFN-γ, 1:1 ratio) for the last 2 days. IL-1β-mediated pathways including IκBα (S32/36), P65 (S536), JNK (T183/Y185), JUN (S63), P38 (T180/Y182), and STAT1 (S727) ratios were examined (n = 3). To normalize, the relative phospho/total ratio of cells without CM stimulation was set at 100%. P values: comparisons between cells stimulated with CM/+IFN-γ and CM/–IFN-γ (#: P < 0.05, ##: P < 0.01 and ###: P < 0.001), or between compound treated and untreated cells (*: P < 0.05, **: P < 0.01 and ***: P < 0.001). (one-way ANOVA with a post hoc Tukey test).