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Updated: Jun 6, 2026
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Effects of agmatine on hypoxic microglia and activity of nitric oxide synthase
Soo Kyung Ahn1, Samin Hong, Yu Mi Park
1Department of Anatomy, Yonsei University College of Medicine, Seoul, Republic of Korea.
Abstract:
Microglia are the resident macrophages of CNS and play a crucial role in maintaining homeostasis against various neuronal injuries. However, excessive activation of microglia may destroy healthy neurons as well as damaged neurons. We investigated neuroprotective effects of amgatine on hypoxic microglia using in vitro and in vivo models for transient hypoxia. For in vitro study, BV2 immortalized murine microglia were incubated with or without 100 μM of agmatine in a closed anaerobic chamber for 2h. After recovery in normoxic condition for 20 h, cell viability and the amount of nitrite generation were determined. For in vivo study, 100mg/kg of agmatine or equivalent volume of saline was intraperitoneally administered, and the left middle cerebral artery of adult male Sprague-Dawley rats was occluded for 90 min. After 24h from occlusion, the cortex and striatum of the forebrains was evaluated to check the immunoreactivity with a microglial marker, ionized calcium binding adaptor molecule 1 (Iba1), and inducible nitric oxide synthase (iNOS). Results showed that agmatine attenuated hypoxia-induced cytotoxicity and nitrite production by BV2 microglia. Agmatine also decreased the activities of microglia and NOS induced by transient middle cerebral artery occlusion. Finally, our findings reveal that agmatine may reduce microglial damages caused by transient hypoxia and suggest that agmatine may lead to a novel therapeutic strategy for hypoxic neuronal injuries.
Insights
Agmatine protects against hypoxic brain injury by reducing microglial activation and nitric oxide production. This suggests agmatine as a potential therapeutic for conditions like stroke.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia, the central nervous system's immune cells, are vital for homeostasis but can cause neuronal damage when overactivated.
- Excessive microglial activation during hypoxic events, such as stroke, contributes to secondary brain injury.
Purpose of the Study:
- To investigate the neuroprotective potential of agmatine against hypoxic injury in microglia.
- To evaluate agmatine's effects on microglial activation and nitric oxide generation in both in vitro and in vivo models of transient hypoxia.
Main Methods:
- In vitro: BV2 murine microglia were exposed to hypoxia with or without agmatine, followed by assessments of cell viability and nitrite production.
- In vivo: Rats underwent transient middle cerebral artery occlusion (MCAO) with agmatine administration, followed by analysis of microglial markers (Iba1) and inducible nitric oxide synthase (iNOS) in brain tissue.
Main Results:
- Agmatine significantly reduced hypoxia-induced cytotoxicity and nitrite generation in BV2 microglia.
- In vivo, agmatine administration decreased microglial activation and iNOS expression following transient MCAO.
Conclusions:
- Agmatine demonstrates neuroprotective effects by mitigating microglial damage and nitric oxide overproduction during transient hypoxia.
- These findings support agmatine as a promising therapeutic candidate for managing hypoxic neuronal injuries, including those resulting from stroke.
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