Fig. 6From: The smoothened agonist SAG reduces mitochondrial dysfunction and neurotoxicity of frataxin-deficient astrocytesChronic treatment with SAG diminishes the inflammatory reactivity phenotype triggered by FXN knockdown in HAs. In A, B, HAs were cultured under standard conditions (untreated) or transduced with either the LV-scrambled or LV-shRNA37 for 96 h, SAG was added daily at 1 μM for 6 days. A The graph on the left shows mRNA expression levels of iNOS and ARG1 represented as the ratio of iNOS/ARG1, the graph in the middle shows expression levels of NFkB and the graph on the right shows expression levels of different pro-inflammatory cytokines determined by qPCR in the indicated treatments. In all cases, gene expression was normalized to the housekeeping gene GAPDH and quantified by the comparative Ct method (n = 4). B The graph on the left shows NRF2 mRNA expression levels and the graph on the right shows mRNA expression levels of genes involved in different neurotrophic pathways, all determined by qPCR. For each gene, the expression was normalized to GAPDH and quantified by the comparative Ct method (n = 4). In all graphs data were normalized (data not plotted) to the untreated group and represent mean values ± S.E.M. In A, B, statistical significance was evaluated by one-way ANOVA followed by Tukey’s post hoc testBack to article page