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

Figure 3 Exosomes secreted by bone marrow mesenchymal stem cells enhance the secretion of inflammatory mediators in hippocampal neurons. A: Confocal microscopy images of HT22 cells co-cultured with bone marrow mesenchymal stem cell-derived exosomes. Cell nuclei were stained with DAPI, cell membranes were stained with CellLINK555, and exosomes were labeled with PKH67. The scale is 25 μm; B: Confocal microscopy imaging was performed after co-culturing HT22 cells with extracellular vesicles from bone marrow mesenchymal stem cells. DAPI staining visualized the cell nuclei, PKH26 staining labeled the cell membrane, and FAM labeling detected miR-203-3p within the extracellular vesicles. The scale bar represents 25 μm; C: Flow cytometry analysis of extracellular vesicles in the supernatant after HT22 cell transfection with FAM-miR-203-3p; D: Electron microscopic examination of extracellular vesicles in the supernatant after HT22 cell transfection with FAM-miR-203-3p; E: Quantitative polymerase chain reaction results reveal a significant increase in miR-203-3p levels in the temporal lobe epilepsy (TLE) group; F: Significant decrease in suppression of cytokine signaling 3 mRNA expression was observed in the TLE group; G-K: Flow cytometric analysis demonstrated an elevated apoptosis rate in the TLE group; L: CCK8 assay indicated reduced cell proliferation in the TLE group; M and N: Enzyme-linked immunosorbent assay detection shows upregulated levels of inflammatory factors such as tumor necrosis factor-α and interleukin-6 in the TLE group. ^bP < 0.01. TLE: Temporal lobe epilepsy; PBS: Phosphate-buffered saline; TNF-α: Tumor necrosis factor-α; IL-6: Interleukin-6.