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Updated: May 19, 2026
Isolation and Intravenous Injection of Murine Bone Marrow Derived Monocytes
Published on: December 27, 2014
Minocycline treatment and bone marrow mononuclear cell transplantation after endothelin-1 induced striatal ischemia
Marcelo M Cardoso1, Edna C S Franco, Celice C de Souza
1Laboratory of Experimental Neuroprotection and Neuroregeneration, Institute of Biological Sciences, Federal University of Pará-Brazil, Rua Augusto Corrêa S/N, Campus do Guamá, 66075-900, Belém, Pará, Brazil.
Abstract:
We explored whether the modulation of microglia activation with minocycline is beneficial to the therapeutic actions of bone marrow mononuclear cells (BMMCs) transplanted after experimental stroke. Male Wistar adult rats were divided in four experimental groups: ischemic control saline treated (G1, N = 6), ischemic minocycline treated (G2, N = 5), ischemic BMMC treated (G3, N = 5), and ischemic minocycline/BMMC treated (G4, N = 6). There was a significant reduction in the number of ED1+ cells in G3 animals (51.31 ± 2.41, P < 0.05), but this effect was more prominent following concomitant treatment with minocycline (G4 = 29.78 ± 1.56). There was conspicuous neuronal preservation in the brains of G4 animals (87.97 ± 4.27) compared with control group (G1 = 47.61 ± 2.25, P < 0.05). The behavioral tests showed better functional recovery in animals of G2, G3, and G4, compared with G1 and baseline (P < 0.05). The results suggest that a proper modulation of microglia activity may contribute to a more permissive ischemic environment contributing to increased neuroprotection and functional recovery following striatal ischemia.
Insights
Minocycline enhances the therapeutic effects of bone marrow mononuclear cells (BMMCs) in stroke recovery by reducing inflammation and preserving neurons. This combined treatment improves functional outcomes in experimental stroke models.
Area of Science:
- Neuroscience
- Immunology
- Regenerative Medicine
Background:
- Stroke induces neuroinflammation, primarily mediated by microglia activation.
- Bone marrow mononuclear cells (BMMCs) show therapeutic potential in stroke but their efficacy can be limited by the inflammatory environment.
- Minocycline is known to modulate microglial activation.
Purpose of the Study:
- To investigate if minocycline-mediated modulation of microglia activation enhances the therapeutic effects of BMMC transplantation in experimental stroke.
- To assess the impact of combined minocycline and BMMC treatment on neuroprotection and functional recovery.
Main Methods:
- Adult male Wistar rats were subjected to experimental stroke and divided into four groups: ischemic control, ischemic minocycline treated, ischemic BMMC treated, and ischemic minocycline/BMMC treated.
- Quantification of microglia activation (ED1+ cells) and neuronal preservation was performed.
- Behavioral tests were conducted to evaluate functional recovery.
Main Results:
- BMMC treatment significantly reduced microglia activation, an effect more pronounced with concomitant minocycline administration.
- Combined minocycline and BMMC treatment led to significantly greater neuronal preservation compared to the control group.
- Animals receiving minocycline, BMMCs, or both showed improved functional recovery compared to controls.
Conclusions:
- Modulating microglia activity with minocycline enhances neuroprotection and functional recovery after experimental striatal ischemia.
- Combined therapy of minocycline and BMMCs creates a more permissive ischemic environment, improving therapeutic outcomes.
