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Minocycline Attenuates Microglia/Macrophage Phagocytic Activity and Inhibits SAH-Induced Neuronal Cell Death and
Kinga G Blecharz-Lang1, Victor Patsouris2, Melina Nieminen-Kelhä2
1Institute of Experimental Neurosurgery, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. kinga.blecharz.lang@gmail.com.
Background:
Neuroprotective treatment strategies aiming at interfering with either inflammation or cell death indicate the importance of these mechanisms in the development of brain injury after subarachnoid hemorrhage (SAH). This study was undertaken to evaluate the influence of minocycline on microglia/macrophage cell activity and its neuroprotective and anti-inflammatory impact 14 days after aneurismal SAH in mice.
Methods:
Endovascular filament perforation was used to induce SAH in mice. SAH + vehicle-operated mice were used as controls for SAH vehicle-treated mice and SAH + minocycline-treated mice. The drug administration started 4 h after SAH induction and was daily repeated until day 7 post SAH and continued until day 14 every second day. Brain cryosections were immunolabeled for Iba1 to detect microglia/macrophages and NeuN to visualize neurons. Phagocytosis assay was performed to determine the microglia/macrophage activity status. Apoptotic cells were stained using terminal deoxyuridine triphosphate nick end labeling. Real-time quantitative polymerase chain reaction was used to estimate cytokine gene expression.
Results:
We observed a significantly reduced phagocytic activity of microglia/macrophages accompanied by a lowered spatial interaction with neurons and reduced neuronal apoptosis achieved by minocycline administration after SAH. Moreover, the SAH-induced overexpression of pro-inflammatory cytokines and neuronal cell death was markedly attenuated by the compound.
Conclusions:
Minocycline treatment may be implicated as a therapeutic approach with long-term benefits in the management of secondary brain injury after SAH in a clinically relevant time window.
Insights
Minocycline reduces brain damage after subarachnoid hemorrhage (SAH) by decreasing microglia/macrophage activity and inflammation. This neuroprotective effect offers potential long-term benefits for managing secondary brain injury following SAH.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Subarachnoid hemorrhage (SAH) triggers inflammation and cell death, crucial in secondary brain injury.
- Neuroprotective strategies targeting these mechanisms are vital for SAH management.
Purpose of the Study:
- To investigate minocycline's effects on microglia/macrophage activity post-SAH.
- To evaluate minocycline's neuroprotective and anti-inflammatory impact 14 days after experimental SAH in mice.
Main Methods:
- Subarachnoid hemorrhage (SAH) induced via endovascular filament perforation in mice.
- Minocycline administered starting 4 hours post-SAH, with varied dosing schedules.
- Immunolabeling for microglia/macrophages (Iba1) and neurons (NeuN), phagocytosis assays, apoptosis staining, and cytokine gene expression analysis.
Main Results:
- Minocycline significantly reduced microglia/macrophage phagocytic activity and their interaction with neurons.
- Neuronal apoptosis and SAH-induced overexpression of pro-inflammatory cytokines were markedly attenuated by minocycline.
- Neuroprotection and anti-inflammatory effects were observed up to 14 days post-SAH.
Conclusions:
- Minocycline demonstrates significant neuroprotective and anti-inflammatory effects in a mouse model of SAH.
- Minocycline may serve as a therapeutic agent for mitigating secondary brain injury after SAH.
- The findings suggest potential long-term benefits of minocycline in a clinically relevant timeframe.
