<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>18(4)</volume><submitter>Zhu XY</submitter><pubmed_abstract>Recent research on the underlying mechanisms of cerebral ischemia indicates that the neurovascular unit can be used as a novel subject for general surveys of neuronal damage and protein mechanisms. Fingolimod (FTY-720) is a newly developed immunosuppressant isolated from Cordyceps sinensis that exhibits a wide range of biological activities, and has recently attracted much attention for the treatment of ischemic cerebrovascular diseases. In the current research, the role of FTY-720 and its possible mechanisms were assessed from an neurovascular unit perspective using a rat cerebral ischemia model. Our results revealed that FTY-720 markedly decreased infarct volume, promoted neurological function recovery, and weakened the blood-brain barrier permeability of ischemic rats. The protective roles of FTY-720 in ischemic stroke are ascribed to a combination of sphingosin-1-phosphate receptor-1 and reduced expression of sphingosin-1-phosphate receptor-1 in microvessels and reduction of interleukin-17A protein levels. These findings indicate that FTY-720 has promise as a new therapy for neurovascular protection and functional recovery after ischemic stroke.</pubmed_abstract><journal>Neural regeneration research</journal><pagination>869-874</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9700117</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Fingolimod protects against neurovascular unit injury in a rat model of focal cerebral ischemia/reperfusion injury.</pubmed_title><pmcid>PMC9700117</pmcid><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Zhao L</pubmed_authors><pubmed_authors>Ma TT</pubmed_authors><pubmed_authors>Liang J</pubmed_authors><pubmed_authors>Zhu XY</pubmed_authors><pubmed_authors>Min LQ</pubmed_authors><pubmed_authors>Zhang MQ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Fingolimod protects against neurovascular unit injury in a rat model of focal cerebral ischemia/reperfusion injury.</name><description>Recent research on the underlying mechanisms of cerebral ischemia indicates that the neurovascular unit can be used as a novel subject for general surveys of neuronal damage and protein mechanisms. Fingolimod (FTY-720) is a newly developed immunosuppressant isolated from Cordyceps sinensis that exhibits a wide range of biological activities, and has recently attracted much attention for the treatment of ischemic cerebrovascular diseases. In the current research, the role of FTY-720 and its possible mechanisms were assessed from an neurovascular unit perspective using a rat cerebral ischemia model. Our results revealed that FTY-720 markedly decreased infarct volume, promoted neurological function recovery, and weakened the blood-brain barrier permeability of ischemic rats. The protective roles of FTY-720 in ischemic stroke are ascribed to a combination of sphingosin-1-phosphate receptor-1 and reduced expression of sphingosin-1-phosphate receptor-1 in microvessels and reduction of interleukin-17A protein levels. These findings indicate that FTY-720 has promise as a new therapy for neurovascular protection and functional recovery after ischemic stroke.</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2025-04-22T09:57:46.457Z</modification><creation>2025-04-05T23:16:50.081Z</creation></dates><accession>S-EPMC9700117</accession><cross_references><pubmed>36204856</pubmed><doi>10.4103/1673-5374.353500</doi></cross_references></HashMap>