Fig. 8

RORα synergizes with miR-7 to control the inflammatory reaction of neuronal cells in vitro. a Neuronal cell PC12 cells were stimulated by 100 ng/mL LPS for 12 h, the expression level of RORα was determined by double immunofluorescence labeling assay. b The expression levels of miR-7 and RORα in neuronal cells were determined by real-time PCR assay and calculated. Neuronal cells were infected with RORα RNAi or NC and then stimulated by 100 ng/mL LPS for 12 h, c–g the expression levels of cytokines (IL-1β, IL-6, TNF-α, and TGF-β) were determined by real-time PCR assay and ELISA assay (n = 7, one-way ANOVA, *P < 0.05, **P < 0.01). h, i The protein levels of signaling molecules including AKT, phos-AKT, ERK1/2, phos-ERK1/2, NF-κB, and phos-NF-κB were determined by Western blot assay and calculated (n = 3, one-way ANOVA; *P < 0.05, **P < 0.01). j Schematic representation of the underlying mechanism of miR-7 and its target molecule RORα synergistically controlled the inflammatory reaction of neurons in response to LPS exposure, which subsequently affected the function of other cells including microglia and astrocytes and ultimately orchestrated the development of BTI