Key result
Macrophage exosome delivery of edaravone boosts bioavailability and reduces neuronal death in ischemic stroke models.
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Edaravone (Edv) can inhibit tissue damage, cause cerebral edema, and delay neuronal death caused by acute cerebral infarction. Exosomes are considered as cargo carriers for intercellular communication and serve as important regulators in many pathological processes. Here, we developed macrophage-derived exosomes (Exo) containing Edv (Exo + Edv) to improve the bioavailability of Edv and enhance the neuroprotective effects in a rat model of permanent middle cerebral artery occlusion (PMCAO). The results showed that Exo + Edv significantly improved the bioavailability of Edv and prolonged half-life ( t 1/2 ). At the same time, Exo + Edv made Edv more easily reach the ischemic side of rats with PMCAO and was localized with neuronal cells and microglia, thus reducing the death of neuronal cells and promoting the polarization of microglia from M1 to M2. Taken together, Exo + Edv may become a potential clinical treatment option for PMCAO.
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Li et al. (2020) studied Permanent middle cerebral artery occlusion (PMCAO) stroke model in rats. Edaravone-loaded macrophage-derived exosomes (Exo + Edv) vs. Edaravone alone was evaluated on Bioavailability of edaravone, neuronal cell death, and microglial M1-to-M2 polarization. Edaravone-loaded macrophage-derived exosomes significantly improved edaravone bioavailability, prolonged half-life, reduced neuronal death, and promoted M1-to-M2 microglial polarization in PMCAO rats.
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