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Updated: May 11, 2026
2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
Bone-marrow mononuclear cells reduce neurodegeneration in hippocampal CA1 layer after transient global ischemia in
Alane Bernardo Ramos1, Andréia Vasconcelos-Dos-Santos, Sergio Augusto Lopes de Souza
1Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. alane@biof.ufrj.br
Insights
Bone-marrow mononuclear cells (BMMCs) transplantation protected hippocampal neurons in a global cerebral ischemia (GCI) model. BMMC treatment reduced neurodegeneration and modulated microglial activation, offering a potential neuroprotective strategy.
Area of Science:
- Neuroscience
- Regenerative Medicine
Background:
- Global cerebral ischemia (GCI) causes pyramidal neuron death in the hippocampus.
- The four-vessel occlusion (4VO) model simulates GCI.
Purpose of the Study:
- Investigate the neuroprotective potential of bone-marrow mononuclear cells (BMMCs) transplantation after GCI.
Main Methods:
- BMMCs were transplanted via carotid artery 1 or 3 days after ischemia in the 4VO model.
- Neurodegeneration was assessed by counting dying cells and FJ-C positive cells at 7 days post-ischemia.
- Microglial activation was evaluated by counting ED1-positive cells.
Main Results:
- BMMC treatment significantly reduced the number of dying cells and FJ-C positive cells in the hippocampal CA1 layer.
- A decrease in activated microglia/macrophages (ED1-positive cells) was observed in BMMC-treated animals.
- Biodistribution studies confirmed cell presence in the hippocampus post-transplantation.
Conclusions:
- BMMC transplantation demonstrates neuroprotective effects in a GCI model.
- BMMCs can modulate the microglial response, reducing neurodegeneration in the hippocampus.
Abstract:
Global cerebral ischemia (GCI) results in death of the pyramidal neurons in the CA1 layer of the hippocampus. In this study we used the four-vessel occlusion (4VO) model of GCI to investigate a potential neuroprotective role of bone-marrow mononuclear cells (BMMCs) transplantation. BMMCs (3×10(7)) were injected through the carotid artery, 1 or 3 days after ischemia (DAI), and the number of cells undergoing degeneration was investigated in brains at 7 DAI. A significant decrease in the number of dying cells was observed in the treated group, compared to animals treated with saline. Biodistribution of the injected cells (1 or 3 DAI) was investigated by (99m)Technetium labeling of the BMMCs and subsequent image analysis 2h after transplantation. In addition, the presence of CellTrace(™)-labeled BMMCs was investigated in tissue sections of the hippocampal area of these transplanted animals. BMMCs treatment significantly reduced the number of FJ-C positive cells in the hippocampal CA1 layer at 7 DAI. We also observed a decrease in the number of activated microglia/macrophage (ED1-positive cells) in the BMMCs-treated group compared with the untreated group. Our data show that BMMCs are able to modulate the microglial response and reduce neurodegeneration in the CA1 layer.
