Exosomal miR-203 from bone marrow stem cells targets the SOCS3/NF-κB pathway to regulate neuroinflammation in temporal lobe epilepsy

Figure 6 Inhibition of the target gene suppression of cytokine signaling 3 can activate the nuclear factor kappaB pathway and promote neuroinflammation. A: Schematic representation of the experimental design for HT22 cells transfected with si-suppression of cytokine signaling 3 (SOCS3) or si-NC, with or without nuclear factor kappaB pathway inhibitor treatment; B: Quantitative polymerase chain reaction analysis of SOCS3 mRNA expression in HT22 cells after transfection; C-J: Western blot analysis of SOCS3 protein levels and nuclear factor kappaB pathway markers in HT22 cells under the same conditions as Figure 6C; K and L: Enzyme-linked immunosorbent assay measurements of interleukin-6 and tumor necrosis factor-α levels in the supernatant of HT22 cells treated as in Figure 6C. Data are presented as mean ± SEM of three independent experiments. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, NS: No significance. SOCS3: Suppression of cytokine signaling 3; NF-κB: Nuclear factor kappaB; IKKα/β: Inhibitor of kappa B kinase alpha/beta; p-IKKα/β: Phospho-inhibitor of kappa B kinase alpha/beta; IKBα: Nuclear factor kappaB inhibitor alpha; p-IKBα: Phospho-nuclear factor kappaB inhibitor alpha; TNF-α: Tumor necrosis factor-α; IL-6: Interleukin-6.