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首页> 外文期刊>Advanced functional materials >A 'Nano-Courier' for Precise Delivery of Acetylcholine and Melatonin by C5a-Targeted Aptamers Effectively Attenuates Reperfusion Injury of Ischemic Stroke
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A 'Nano-Courier' for Precise Delivery of Acetylcholine and Melatonin by C5a-Targeted Aptamers Effectively Attenuates Reperfusion Injury of Ischemic Stroke

机译：A 'Nano-Courier' for Precise Delivery of Acetylcholine and Melatonin by C5a-Targeted Aptamers Effectively Attenuates Reperfusion Injury of Ischemic Stroke

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Overactive inflammatory response and excessive oxidative stress are the mainpathophysiological culprits for cerebral ischemia/reperfusion injury (IRI) thatarouse neuronal damage . The neurotransmitter acetylcholine (ACh) exerts antiinflammatoryroles by stimulating α7 nicotinic acetylcholine receptor (α7nAChR)on microglia to activate the cholinergic anti-inflammatory pathway. Simultaneously,as a circadian rhythm-dependent hormone , melatonin (MT) possessespromising neuroprotective effects that eliminate reactive oxygen species (ROS)in the ischemic region. Relying on these, a biocompatible fluorescein isothiocyanate(FITC)-labeled SiO_2@PAA-MT/Ach nanospheres are constructed to effectivelyalleviate oxidative stress and polarize microglial phenotype to suppressinflammatory response in cerebral IRI. Despite of biosafety and curative effectsof Ach and MT, the poor aggregation in ischemic penumbra hinders theirneuroprotection. To address that, complement component 5a (C5a) is used asa molecular target for delivery of Ach and MT. C5a conspicuously exists at localinflammatory sites of cerebral IRI, recruits immune cells, and mediates furtherrelease of inflammatory cytokines. Upon binding of anti-C5a (aC5a) aptamersonto FITC-labeled SiO2@PAA-MT/Ach nanospheres, they can effectively targetthe ischemic penumbra and promote neurological recovery. Taken together, thecurrent study suggests that the FITC-labeled SiO_2@PAA-MT/Ach-aC5a nanospheresafter intravenous (i.v.) administration can act as an effective targetednanotherapy to salvage neurons in cerebral IRI.

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