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Updated: May 16, 2026
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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
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Multiaspect layered double hydroxide nanohybrid counteracts pathophysiological cascade for ischemic stroke
Yize Dong1, Yihong Su1, Guangjie Sun1
1Department of Radiology, Gongli Hospital of Shanghai Pudong New Area, Shanghai 200135, China.
Summary
A novel nanosheet platform (S-E@LDH) effectively treats ischemic stroke (IS) by targeting calcium dysregulation, oxidative stress, and inflammation. This therapy reduces brain damage and improves motor function in mice.
Area of Science:
- Biomedical Engineering
- Nanomedicine
- Neuroscience
Background:
- Ischemic stroke (IS) therapy is complicated by ischemia-reperfusion injury.
- Existing treatments struggle to address the multifaceted pathology of IS.
Purpose of the Study:
- To develop a hybrid nanosheet platform (S-E@LDH) for synergistic regulation of calcium dysregulation, oxidative stress, and inflammation in IS.
- To investigate the therapeutic efficacy of S-E@LDH in a mouse model of transient IS.
Main Methods:
- Fabrication of a layered double hydroxide (LDH) nanosheet matrix incorporating MgAlRu, ethylene glycol tetraacetic acid (EGTA), and salvianic acid A (SAA).
- In vitro assessment of chelating Ca2+, scavenging reactive oxygen/nitrogen species, and disrupting Ca2+-ROS amplification.
- In vivo evaluation in a mouse model of transient IS, assessing neuronal damage, neuroinflammation, cerebral edema, and motor function.
Main Results:
- S-E@LDH effectively chelated Ca2+, scavenged reactive oxygen/nitrogen species, and disrupted the Ca2+-ROS amplification loop.
- Spatiotemporally controlled release of SAA reprogrammed microglia to an M2 phenotype, restoring brain homeostasis.
- S-E@LDH treatment significantly reduced neuronal damage, neuroinflammation, and cerebral edema, leading to improved motor function in IS mice.
Conclusions:
- The S-E@LDH nanosheet platform offers a multi-targeted, spatiotemporally controlled therapeutic strategy for IS.
- This approach effectively addresses the complex pathogenesis of IS by simultaneously targeting key pathological pathways.
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