Fig. 6

Mitochondrial depletion abolishes the therapeutic effect of UMSCs on neurological deficits and peripheral immune microenvironment in MCAO mouse models. A RT-qPCR analysis of mtDNA expression in UMSCs during ddC depletion. B Experimental design for UMSCs treatment in experimental ischemic stroke. The experiment included four groups: sham surgery, MCAO, MCAO + UMSC treatment, and MCAO + UMSC (ddC) treatment (N = 5/group). Brain tissues were collected for TTC staining, spleens were harvested and weighed, and peripheral T cells and plasma were isolated for T cell phenotype and cytokine analysis. Data are presented as scatter plots with median values and IQR. Severity and recovery of sensorimotor deficits after cerebral focal ischemia were assessed using the Longa test (C) and cylinder test (D). (E) TTC staining of brain slices 3 days post-ischemia (white indicates the infarct area), with quantification of infarct volume based on relative proportion from TTC staining. F Comparison of spleen weights across different treatment groups. G Representative flow plot and frequencies of Tcell subsets in different treatment groups, expressed as percentages of total CD45⁺ cells. H Representative flow plot and frequencies of Th17 and Treg cells, expressed as percentages of total CD4⁺ T cells. I Comparison of Th17/Treg cell ratio among groups. J IL-6 concentration in different mouse model groups. K Flow histogram and ROS expression in total T cell across different groups. Except for additional annotations, data are presented as scatter plots with mean values and SD. Statistical comparisons were performed using repeated measures analysis of variance, one-way ANOVA with Tukey's post hoc test, Welch’s t-test with Dunnett’s post hoc test, or the Kruskal–Wallis test, with p < 0.05 considered statistically significant. *p < 0.05, **p < 0.01, and ***p < 0.001. Abbreviations: mtDNA, mitochondrial DNA; MCAO, middle cerebral artery occlusion