Fig. 8

BMSCs-derived exosomal miR-138-5p reduces neuron injury following IS in vivo. a, HE staining for hippocampal tissues of MCAO mouse models (scale bar = 25 μm); b, TUNEL staining to detect neuron apoptosis (scale bar = 25 μm) and quantitative analysis for the apoptotic rate; c, TTC staining showing the volume changes of cerebral infarction in mice and the corresponding quantitative analysis; d, Nissl staining (scale bar = 50 μm) showing the number of neurons and the corresponding quantitative analysis; e, quantitative analysis for LDH content; f, protein expression of inflammatory factors, proliferation and apoptosis marker proteins determined by Western blot analysis. The data were all measurement data, expressed as mean ± standard deviation. The comparison among multiple groups was analyzed by one-way analysis of variance. The experiment was repeated three times. *, p < 0.05 vs. sham. #, p < 0.05 vs. MCAO. n = 10. LDH, lactate dehydrogenase; TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling; MCAO, middle cerebral artery occlusion; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; Bax, Bcl-2-associated X protein; Bcl-2, B-cell CLL/Lymphoma 2; IL-6, interleukin-6; IL-1β, interleukin-1β; TNF-α, tumor necrosis factor-α; BMSCs-control, MCAO mice without any treatment; BMSCs-miR-NC, MCAO mice injected with BMSCs-miR-NC exosomes; BMSCs-miR-138-5p, MCAO mice injected with BMSCs-miR-138-5p exosomes