Journal: Brain and Behavior

Article Title: Human Umbilical Cord Blood Mesenchymal Stem Cells Ameliorate Autism‐Like Behaviors in a Valproic Acid‐Induced Mouse Model via the IGF‐1/Akt Signaling Pathway

doi: 10.1002/brb3.71335

Figure Lengend Snippet: The hUC‐MSCs treatment significantly attenuates autism‐spectrum behaviors in VPA‐induced mice. (A) Flow chart for the study procedure. (B) Three‐chamber test; n = 14 (control), 13 (VPA), 22 (MSCs). (C) Duration of sociability. (D) Duration of social novelty. (E) Marbles bury test; n = 14 (control), 11 (VPA), 15 (MSCs). (F) The open field test; n = 14 (control), 11 (VPA), 15 (MSCs). (G–I) The total distance, average speed, and center duration were analyzed for comparison. Results are shown as mean ± SEM. * p < 0.05; ** p < 0.01; NS means not significant.

Article Snippet: The hUC‐MSCs were supplied by Beike Biotechnology.

Techniques: Control, Comparison

Journal: Brain and Behavior

Article Title: Human Umbilical Cord Blood Mesenchymal Stem Cells Ameliorate Autism‐Like Behaviors in a Valproic Acid‐Induced Mouse Model via the IGF‐1/Akt Signaling Pathway

doi: 10.1002/brb3.71335

Figure Lengend Snippet: hUC‐MSCs promote the development of cortical neuronal dendrites. (A) Golgi staining of the cortical neurons. The scale bar represents 5 µm at 100× magnification. (B) The dendritic spine within 24 dendritic segments from three mice in each group were quantitatively analyzed. (C) Representative images of primary cultured neurons are shown with MAP2 in green, GFAP in red, and DAPI in blue. The scale bar represents 100 µm at 10× magnification. (D) Immunofluorescence staining of MAP2 in primary neurons co‐cultured with hUC‐MSCs‐CM is shown; scale bars represent 50 µm at 20× magnification and 20 µm at 40× magnification. (E) Sholl analysis was used to evaluate the dendritic complexity of cortical neurons, with 12 neurons analyzed from three mice per group. Data are presented as mean ± SEM. * p < 0.05; ** p < 0.01; NS indicates not significant.

Article Snippet: The hUC‐MSCs were supplied by Beike Biotechnology.

Techniques: Staining, Cell Culture, Immunofluorescence

Journal: Brain and Behavior

Article Title: Human Umbilical Cord Blood Mesenchymal Stem Cells Ameliorate Autism‐Like Behaviors in a Valproic Acid‐Induced Mouse Model via the IGF‐1/Akt Signaling Pathway

doi: 10.1002/brb3.71335

Figure Lengend Snippet: In the cerebral cortex of VPA‐induced ASD mice, hUC‐MSCs transplantation normalizes p‐IGF‐1R/IGF‐1R and p‐Akt/Akt ratios, enhances neuronal development gene expression, and suppresses inflammation and apoptosis‐related gene expression. (A) Representative immunoblots and quantitative analysis of phosphorylated IGF‐1R (p‐IGF‐1R) and total IGF‐1R protein levels in cortical tissue lysates. The ratio of p‐IGF‐1R to total IGF‐1R was determined by densitometry ( n = 3 per group). (B) Representative immunoblots and quantitative analysis of phosphorylated Akt (p‐Akt) and total Akt protein levels in cortical tissue lysates ( n = 3 per group). (C) Quantification of mRNA levels for GAP‐43, SYP, Caspase‐3, Bax, IL‐6, IL‐1β, and IL‐10 in the cortex ( n = 6 per group). Data are presented as mean ± SEM, with each dot on the graph representing an individual biological replicate. * p < 0.05; ** p < 0.01; NS indicates not significant.

Article Snippet: The hUC‐MSCs were supplied by Beike Biotechnology.

Techniques: Transplantation Assay, Gene Expression, Western Blot

Journal: Brain and Behavior

Article Title: Human Umbilical Cord Blood Mesenchymal Stem Cells Ameliorate Autism‐Like Behaviors in a Valproic Acid‐Induced Mouse Model via the IGF‐1/Akt Signaling Pathway

doi: 10.1002/brb3.71335

Figure Lengend Snippet: The hUC‐MSCs shows no clear in vivo toxicity. (A) Representative micrographs of H&E‐stained sections 2 weeks after surgery; scale bars represent 100 µm at 10× magnification and 20 µm at 40× magnification. (B,C) Average body weight of each group 2 weeks after surgery. n = 7 (control), 7 (VPA), 7 (MSCs). Data are presented as mean ± SEM. * p < 0.05; ** p < 0.01; NS indicates not significant.

Article Snippet: The hUC‐MSCs were supplied by Beike Biotechnology.

Techniques: In Vivo, Staining, Control

Journal: Alzheimer's Research & Therapy

Article Title: hUC-MSC-derived exosomes ameliorate Alzheimer's disease pathology through lncRNA-9969-mediated multi-target protection involving neuronal autophagy and microglial modulation

doi: 10.1186/s13195-026-01954-4

Figure Lengend Snippet: LncRNA-9969 in hUC-MSC-derived exosomes alleviates Aβ-induced neuronal injury by regulating the mTOR-autophagy pathway. A Transmission electron microscopy of hUC-MSC-derived exosomes (scale bars: 100 nm, 500 nm). B TUNEL staining of SH-SY5Y cells under different treatments, with quantification of TUNEL-positive signals. C Aβ aggregation detected by immunofluorescence, with quantification of Aβ-positive signal intensity (scale bar: 50 μm). D Western blot analysis of APP, SYN, pro-BDNF, p-mTOR, p-p70S6K, Beclin1, and LC3B, with corresponding quantification. Experimental groups: SH, control group; SH + Aβ 25–35 , Aβ 25–35 injury group; SH + Aβ 25–35 + MSCs, Aβ 25–35 injury + wild-type hUC-MSC-derived exosome treatment group; SH + Aβ 25–35 + MSC-lncRNA, Aβ 25–35 injury + lncRNA-9969 knockdown hUC-MSC-derived exosome treatment group. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 ; ns, not significant

Article Snippet: Experimental groups: SH, control group; SH + Aβ 25–35 , Aβ 25–35 injury group; SH + Aβ 25–35 + MSCs, Aβ 25–35 injury + wild-type hUC-MSC-derived exosome treatment group; SH + Aβ 25–35 + MSC-lncRNA, Aβ 25–35 injury + lncRNA-9969 knockdown hUC-MSC-derived exosome treatment group.

Techniques: Derivative Assay, Transmission Assay, Electron Microscopy, TUNEL Assay, Staining, Immunofluorescence, Western Blot, Control, Knockdown

Journal: Alzheimer's Research & Therapy

Article Title: hUC-MSC-derived exosomes ameliorate Alzheimer's disease pathology through lncRNA-9969-mediated multi-target protection involving neuronal autophagy and microglial modulation

doi: 10.1186/s13195-026-01954-4

Figure Lengend Snippet: LncRNA-9969 deficiency reduces the ability of hUC-MSC-derived exosomes to improve cognitive and behavioral performance in AD mice. A Morris water maze assessing spatial learning and memory. Representative swimming trajectories are shown. Quantitative analyses include: percentage of path length in the target quadrant, latency to first target entry, percentage of time spent in the target quadrant, and the Day-7 escape latency for each mouse ( n = 10 per group). B Y-maze test assessing short-term working memory. Representative trajectories are shown. Quantitative analyses include: percentage of distance traveled in the novel arm, latency to first novel-arm entry, percentage of time spent in the novel arm, and Day-7 latency to first novel-arm entry for each mouse ( n = 10 per group). C Open field test evaluating anxiety-like behavior and locomotion. Representative movement paths are shown. Quantitative analyses include: percentage of distance traveled in the central zone, latency to first center entry, percentage of time spent in the central zone, and Day-7 center-zone latency for each mouse ( n = 6 per group). Experimental groups: WT (wild-type control); AD (AD mice receiving PBS); AD + MSCs (AD mice receiving wild-type hUC-MSC exosomes); AD + MSC-lncRNA (AD mice receiving lncRNA-9969 knockdown exosomes). Data are mean ± SEM; one-way ANOVA with Tukey’s post-hoc test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 ; ns, not significant

Article Snippet: Experimental groups: SH, control group; SH + Aβ 25–35 , Aβ 25–35 injury group; SH + Aβ 25–35 + MSCs, Aβ 25–35 injury + wild-type hUC-MSC-derived exosome treatment group; SH + Aβ 25–35 + MSC-lncRNA, Aβ 25–35 injury + lncRNA-9969 knockdown hUC-MSC-derived exosome treatment group.

Techniques: Derivative Assay, Control, Knockdown

Journal: Alzheimer's Research & Therapy

Article Title: hUC-MSC-derived exosomes ameliorate Alzheimer's disease pathology through lncRNA-9969-mediated multi-target protection involving neuronal autophagy and microglial modulation

doi: 10.1186/s13195-026-01954-4

Figure Lengend Snippet: hUC-MSC-derived exosomes ameliorate pathological changes in the brains of AD mice through regulation of autophagy, with lncRNA-9969 as a critical mediator. A Western blot analysis of hippocampal proteins, including APP, SYN, pro-BDNF, and autophagy-related markers (p-mTOR, p-p70S6K, Beclin1, LC3B, P62), with GAPDH as the loading control. Corresponding quantitative analyses of protein expression are shown. B Immunohistochemical staining of hippocampal sections for Aβ, SYN, and BDNF, with quantification of positive staining areas. C Transmission electron microscopy of hippocampal ultrastructure, showing representative mitochondrial morphology; mitochondrial number per field is quantified (scale bar: 1 μm). D Immunohistochemical staining for autophagy markers (P62, Beclin1, LC3B), with quantification of positive staining areas. Data are presented as mean ± SEM ( n = 3). Statistical analysis was performed by one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 ; ns, not significant

Article Snippet: Experimental groups: SH, control group; SH + Aβ 25–35 , Aβ 25–35 injury group; SH + Aβ 25–35 + MSCs, Aβ 25–35 injury + wild-type hUC-MSC-derived exosome treatment group; SH + Aβ 25–35 + MSC-lncRNA, Aβ 25–35 injury + lncRNA-9969 knockdown hUC-MSC-derived exosome treatment group.

Techniques: Derivative Assay, Western Blot, Control, Expressing, Immunohistochemical staining, Staining, Transmission Assay, Electron Microscopy