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Microglia Attenuate Neuroinflammation After Subarachnoid Hemorrhage by Modulating Astrocyte Phenotypic Transformation
Yuxiao Meng1, Yuanzhe Dong1, Jiang Shao2
1Department of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin, 150000, China.
Molecular Neurobiology
|June 4, 2026
Summary
Retinoic acid receptor alpha (RARα) activation reduces brain inflammation after subarachnoid hemorrhage (SAH) by controlling microglia-astrocyte communication. This approach improves neurological function and offers a new therapeutic target for SAH recovery.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia-astrocyte interactions drive neuroinflammation and secondary brain injury post-subarachnoid hemorrhage (SAH).
- Retinoic acid receptor alpha (RARα) shows potential in modulating neuroinflammation, but its role in SAH-related microglial-astrocytic crosstalk is unclear.
Purpose of the Study:
- To investigate if RARα activation alleviates neuroinflammation after SAH by regulating microglial-astrocytic crosstalk via the Mafb/Msr1/PI3K-Akt signaling axis.
- To explore RARα as a potential therapeutic target for improving outcomes after SAH.
Main Methods:
- Established an in vivo SAH rat model and an in vitro microglia-astrocyte co-culture system treated with oxyhemoglobin.
- Administered the RARα agonist Am80 and pathway-specific inhibitors.
- Evaluated molecular markers (Mafb, Msr1, PI3K/Akt), cytokines, glial activation, and neurobehavioral outcomes.
Main Results:
- RARα activation with Am80 significantly attenuated neuroinflammation and improved neurological function in SAH rats.
- Am80 upregulated Mafb and Msr1, activating the PI3K/Akt pathway, which inhibited NF-κB-mediated inflammation and boosted anti-inflammatory factors.
- Blocking PI3K/Akt or reducing Mafb/Msr1 abolished Am80's anti-inflammatory effects, confirming the pathway's importance.
Conclusions:
- RARα activation mitigates SAH-induced neuroinflammation by modulating microglial-astrocyte interactions through the Mafb/Msr1/PI3K-Akt pathway.
- RARα represents a promising therapeutic target for ameliorating neuroinflammation and enhancing recovery following SAH.
