Polydopamine-Cloaked Nanoarchitectonics of Prussian Blue Nanoparticles Promote Functional Recovery in Neonatal and Adult Ischemic Stroke Models.
Yijing ZhaoCong SongHaijun WangChengcheng GaiTingting LiYahong ChengJunjie LiuYan SongQian LuoBing GuWeiyang LiuLiwei ChaiDexiang LiuZhen WangPublished in: Biomaterials research (2024)
Ischemic stroke is a devastating disease and one of the leading causes of mortality worldwide. Overproduction of reactive oxygen species and inflammatory response contribute to secondary damage following ischemic insult. Nanozymes with robust anti-oxidative stress properties possess therapeutic possibility for ischemic insult. However, insufficiency of nanozyme accumulation in the neuronal mitochondria hindered their application. Herein, we constructed polydopamine-coated Prussian blue nanoparticles (PB@PDA NPs) to realize the targeting neuronal mitochondria for ischemic stroke, with the properties of antioxidant and anti-inflammation. After administration, much higher accumulation of PB@PDA NPs in the brain was observed compared to that in the PB NP group. Moreover, PB@PDA NPs effectively attenuated brain infarct than that of PB NPs in neonatal mice following hypoxia-ischemia (HI) insult. PB@PDA NPs mainly colocated with neuronal mitochondria in vivo and in vitro. Apart from attenuating oxidative stress, PB@PDA NPs also suppressed neuronal apoptosis and counteracted inflammation, which effectively promote a short- and long-term functional recovery in HI mice. Further, the therapeutic efficacy of PB@PDA NPs was also found in adult ischemic mice via tail vein injection. Collectively, these findings illustrate that PB@PDA NPs via system injection accumulate in neuronal mitochondria and are beneficial for ischemic stroke.
Keyphrases
- oxidative stress
- heavy metals
- cerebral ischemia
- reactive oxygen species
- aqueous solution
- ischemia reperfusion injury
- inflammatory response
- oxide nanoparticles
- cell death
- atrial fibrillation
- dna damage
- diabetic rats
- high fat diet induced
- cardiovascular disease
- subarachnoid hemorrhage
- blood brain barrier
- induced apoptosis
- white matter
- heart failure
- resting state
- brain injury
- metabolic syndrome
- young adults
- risk factors
- cancer therapy
- endoplasmic reticulum
- lipopolysaccharide induced
- cell proliferation
- cardiovascular events
- ultrasound guided
- lps induced
- heat shock
- magnetic nanoparticles
- pi k akt