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Related Experiment Video

Updated: Jul 16, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Covalent organic framework based cytoprotective therapy after ischemic stroke.

Yuqin Peng¹, Qingfan Ren², Huanrong Ma³

¹Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.

|March 5, 2024

Summary

This study developed a novel drug delivery system using covalent organic frameworks (COFs) to improve cytoprotection for acute ischemic stroke (AIS). The S/G@COF therapy effectively reduced brain damage by targeting reactive oxygen species (ROS) and SUR1-TRPM4 channels.

Keywords:

Covalent organic framework Cytoprotective therapy Glyburide Ischemic stroke Sulfonylurea receptor 1-transient receptor potential M4

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Area of Science:

Neuroscience
Biomaterials Science
Pharmacology

Background:

Acute ischemic stroke (AIS) causes significant brain injury, often exacerbated by reactive oxygen species (ROS) and the SUR1-TRPM4 channel.
Current treatments face limitations due to low bioavailability of drugs like glyburide (GLB).

Purpose of the Study:

To develop a novel drug delivery system to enhance cytoprotection for AIS.
To overcome the bioavailability issues of GLB and mitigate ROS-induced damage.

Main Methods:

Glyburide (GLB) and superoxide dismutase (SOD) were encapsulated within a stable, porous covalent organic framework (COF), creating S/G@COF.
The therapeutic efficacy of S/G@COF was evaluated in models of AIS, assessing neurological function, brain edema, neuroinflammation, and BBB integrity.

Main Results:

S/G@COF significantly improved survival rates and neurological functions in AIS models.
The treatment effectively eliminated ROS, reduced neuronal loss and apoptosis, suppressed neuroinflammation, modulated microglia activation, and ameliorated blood-brain barrier disruption.
Mechanistic studies showed S/G@COF activated the Wnt/β-catenin pathway while downregulating SUR1-TRPM4.

Conclusions:

Drug modification using COFs offers a promising strategy for enhancing cytoprotection in AIS.
S/G@COF demonstrates multi-target therapeutic potential for ischemic stroke treatment.