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Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway
Meng-Meng Zhu1, Tian-Xiao Li1, Xue-Ting Liu1
1Department of Neurology, School of Medicine, Southeast University, #87 Dingjiaqiao Road, Nanjing, Jiangsu 210009, China.
Iscience
|May 11, 2026
Summary
Propranolol reduces brain injury after ischemic stroke by inhibiting microglial activation and NLRP3 inflammasome. This beta-adrenergic receptor blocker protects the blood-brain barrier and reduces inflammation.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Ischemic stroke causes significant brain injury and inflammation.
- Microglial activation and NLRP3 inflammasome play critical roles in stroke pathophysiology.
- Beta-adrenergic receptors (β-AR) are implicated in inflammatory responses.
Purpose of the Study:
- To investigate the neuroprotective effects of propranolol in ischemic stroke.
- To elucidate the role of β2-AR signaling in stroke-related inflammation and brain injury.
Main Methods:
- Transient middle cerebral artery occlusion (tMCAO) in mice and oxygen-glucose deprivation (OGD) in BV2 cells.
- Behavioral, biochemical, and pathological analyses, including Evans blue extravasation.
- Assessment of microglial activation, NLRP3, IL-1β, p-ERK1/2, and tight junction proteins (Occludin, ZO-1).
Main Results:
- Propranolol alleviated brain injury, reduced microglial activation, and decreased NLRP3 and IL-1β expression.
- Propranolol reduced Evans blue extravasation and enhanced blood-brain barrier integrity markers (Occludin, ZO-1, CD-31).
- β2-AR blockade and U0126 treatment inhibited p-ERK1/2 and NLRP3 expression in OGD-treated BV2 cells.
Conclusions:
- Propranolol exerts neuroprotective effects in ischemic stroke by modulating microglial activation and NLRP3 inflammasome.
- β2-AR signaling is crucial in regulating the inflammatory response and brain injury following ischemic stroke.
- Targeting β2-AR signaling represents a potential therapeutic strategy for ischemic stroke.
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