Article Figures & Data
Figures
- Figure 1
Schematic representation of key mechanisms underlying ischaemic injuries after stroke. DAMPs, damage-associated molecular pattern molecules; GABAAR, γ-aminobutyric acid A receptor; NMDAR, N-methyl-D-aspartate receptor; nNOS, neuronal nitric oxide synthase; NO, nitric oxide; PSD-95, postsynaptic density 95; RNS, reactive nitrogen species; ROS, reactive oxygen species. (+) activation, (−) inhibition.
- Figure 2
Schematic representation of key mechanisms underlying reperfusion-induced injuries after stroke. BBB, blood–brain barrier; HT, haemorrhagic transformation; I/R, ischaemia/reperfusion; RNS, reactive nitrogen species; ROS, reactive oxygen species.
- Figure 3
Reperfusion and cytoprotective agents are a mutually beneficial pair for the outcomes of acute ischaemic stroke. Reperfusion not only improve the outcome of ischaemic stroke but also provides a physiological environment for cytoprotective agents to function. Cytoprotective agents extend the time window for reperfusion therapy by ‘freezing’ ischaemic penumbra when used before reperfusion, and reduce reperfusion injuries when used after reperfusion.
