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Therapeutic potential of human amniotic membrane-derived mesenchymal stem cells in APP transgenic mice

View Article: PubMed Central - PubMed

ABSTRACT

Growing evidence indicates that the presence of extensive oxidative stress plays an essential role in the initiation and progression of Alzheimer's disease (AD). Amyloid-β (Aβ) aggregation is involved in the elevation of oxidative stress, contributing to mitochondrial dysfunction and lipid peroxidation. In the present study, human placenta amniotic membrane-derived mesenchymal stem cells (hAMMSCs) were intravenously injected into C57BL/6J-APP transgenic mice. hAMMSCs significantly ameliorated spatial learning and memory function, and were associated with a decreased amount of amyloid plaques of the brain. The correlation of oxidative stress with Aβ levels was lower in the hAMMSCs-injected group than in the phosphate-buffered saline (PBS)-injected group, as indicated by the increased level of antioxidative enzymes and the decreased level of lipid peroxidation product. The glutathione (GSH) level and ratio of GSH to glutathione disulfide were higher in the hAMMSC group than in the PBS group. The superoxide dismutase activity and malonaldehyde level were improved significantly as the level of Aβ decreased, but there was no such trend in the PBS group. As a result, our findings represent evidence that hAMMSC treatment might improve the pathology of AD and memory function through the regulation of oxidative stress.

No MeSH data available.


Related in: MedlinePlus

Human amniotic membrane-derived mesenchymal stem cell (AMMSC) treatment attenuates amyloid-β (Aβ) deposition in the brains of Alzheimer's disease (AD) transgenic mice. (A) Plaques of the cerebral cortex and hippocampus were observed by Congo red staining (scale bar: 200 µm). (B) Morphometric analysis was performed to qualify the plaques in the cortex and hippocampus. *P<0.05 vs. phosphate-buffered saline (PBS) group.
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f3-ol-0-0-4857: Human amniotic membrane-derived mesenchymal stem cell (AMMSC) treatment attenuates amyloid-β (Aβ) deposition in the brains of Alzheimer's disease (AD) transgenic mice. (A) Plaques of the cerebral cortex and hippocampus were observed by Congo red staining (scale bar: 200 µm). (B) Morphometric analysis was performed to qualify the plaques in the cortex and hippocampus. *P<0.05 vs. phosphate-buffered saline (PBS) group.

Mentions: Since Aβ deposition is the main pathogenic cause of AD inducing cognitive deficits, brain tissue excised from mice following the water maze test was incubated with anti-Aβ 6E10 antibody to observe the changes in Aβ deposition. hAMMSC transplantation notably decreased the Aβ plaques in the cortex and hippocampus of mice compared with the PBS-injected control group (Fig. 3A). Plaque load was qualified by morphometric analysis and is shown as the percentage of the total area demonstrating immunoreactivity of Aβ. The PBS-treated AD mice demonstrated severe Aβ deposition with plaque levels of 60% and 49% in the cortex and hippocampus, whereas the hAMMSC group demonstrated a reduced plaque load of 22% and 14% in the cortex and hippocampus (Fig. 3B).


Therapeutic potential of human amniotic membrane-derived mesenchymal stem cells in APP transgenic mice
Human amniotic membrane-derived mesenchymal stem cell (AMMSC) treatment attenuates amyloid-β (Aβ) deposition in the brains of Alzheimer's disease (AD) transgenic mice. (A) Plaques of the cerebral cortex and hippocampus were observed by Congo red staining (scale bar: 200 µm). (B) Morphometric analysis was performed to qualify the plaques in the cortex and hippocampus. *P<0.05 vs. phosphate-buffered saline (PBS) group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998013&req=5

f3-ol-0-0-4857: Human amniotic membrane-derived mesenchymal stem cell (AMMSC) treatment attenuates amyloid-β (Aβ) deposition in the brains of Alzheimer's disease (AD) transgenic mice. (A) Plaques of the cerebral cortex and hippocampus were observed by Congo red staining (scale bar: 200 µm). (B) Morphometric analysis was performed to qualify the plaques in the cortex and hippocampus. *P<0.05 vs. phosphate-buffered saline (PBS) group.
Mentions: Since Aβ deposition is the main pathogenic cause of AD inducing cognitive deficits, brain tissue excised from mice following the water maze test was incubated with anti-Aβ 6E10 antibody to observe the changes in Aβ deposition. hAMMSC transplantation notably decreased the Aβ plaques in the cortex and hippocampus of mice compared with the PBS-injected control group (Fig. 3A). Plaque load was qualified by morphometric analysis and is shown as the percentage of the total area demonstrating immunoreactivity of Aβ. The PBS-treated AD mice demonstrated severe Aβ deposition with plaque levels of 60% and 49% in the cortex and hippocampus, whereas the hAMMSC group demonstrated a reduced plaque load of 22% and 14% in the cortex and hippocampus (Fig. 3B).

View Article: PubMed Central - PubMed

ABSTRACT

Growing evidence indicates that the presence of extensive oxidative stress plays an essential role in the initiation and progression of Alzheimer's disease (AD). Amyloid-&beta; (A&beta;) aggregation is involved in the elevation of oxidative stress, contributing to mitochondrial dysfunction and lipid peroxidation. In the present study, human placenta amniotic membrane-derived mesenchymal stem cells (hAMMSCs) were intravenously injected into C57BL/6J-APP transgenic mice. hAMMSCs significantly ameliorated spatial learning and memory function, and were associated with a decreased amount of amyloid plaques of the brain. The correlation of oxidative stress with A&beta; levels was lower in the hAMMSCs-injected group than in the phosphate-buffered saline (PBS)-injected group, as indicated by the increased level of antioxidative enzymes and the decreased level of lipid peroxidation product. The glutathione (GSH) level and ratio of GSH to glutathione disulfide were higher in the hAMMSC group than in the PBS group. The superoxide dismutase activity and malonaldehyde level were improved significantly as the level of A&beta; decreased, but there was no such trend in the PBS group. As a result, our findings represent evidence that hAMMSC treatment might improve the pathology of AD and memory function through the regulation of oxidative stress.

No MeSH data available.


Related in: MedlinePlus