<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liang H</submitter><funding>National Natural Science Foundation of China</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>61</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7206796</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>27(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The disruption of the blood-brain barrier (BBB) plays a critical event in the pathogenesis of ischemia stroke. TGR5 is recognized as a potential target for the treatment for neurologic disorders.&lt;h4>Methods&lt;/h4>This study investigated the roles of TGR5 activation in attenuating BBB damage and underlying mechanisms after middle cerebral artery occlusion (MCAO). Sprague-Dawley rats were subjected to model of MCAO and TGR5 agonist, INT777, was administered intranasally. Small interfering RNA (siRNA) for TGR5 and BRCA1 were administered through intracerebroventricular injection 48 h before MCAO. Infarct volumes, brain water content, BBB permeability, neurological scores, Western blot, immunofluorescence staining and co- immunoprecipitation were evaluated.&lt;h4>Results&lt;/h4>Endo</pubmed_abstract><journal>Journal of biomedical science</journal><pubmed_title>Activation of TGR5 protects blood brain barrier via the BRCA1/Sirt1 pathway after middle cerebral artery occlusion in rats.</pubmed_title><pmcid>PMC7206796</pmcid><funding_grant_id>NS081740</funding_grant_id><funding_grant_id>NS082184</funding_grant_id><funding_grant_id>81671143</funding_grant_id><pubmed_authors>McBride DW</pubmed_authors><pubmed_authors>Tang J</pubmed_authors><pubmed_authors>Liang H</pubmed_authors><pubmed_authors>Zhang JH</pubmed_authors><pubmed_authors>Matei N</pubmed_authors><pubmed_authors>Luo B</pubmed_authors><pubmed_authors>Xu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Activation of TGR5 protects blood brain barrier via the BRCA1/Sirt1 pathway after middle cerebral artery occlusion in rats.</name><description>&lt;h4>Background&lt;/h4>The disruption of the blood-brain barrier (BBB) plays a critical event in the pathogenesis of ischemia stroke. TGR5 is recognized as a potential target for the treatment for neurologic disorders.&lt;h4>Methods&lt;/h4>This study investigated the roles of TGR5 activation in attenuating BBB damage and underlying mechanisms after middle cerebral artery occlusion (MCAO). Sprague-Dawley rats were subjected to model of MCAO and TGR5 agonist, INT777, was administered intranasally. Small interfering RNA (siRNA) for TGR5 and BRCA1 were administered through intracerebroventricular injection 48 h before MCAO. Infarct volumes, brain water content, BBB permeability, neurological scores, Western blot, immunofluorescence staining and co- immunoprecipitation were evaluated.&lt;h4>Results&lt;/h4>Endo</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 May</publication><modification>2025-04-22T00:53:09.154Z</modification><creation>2020-05-22T20:09:10Z</creation></dates><accession>S-EPMC7206796</accession><cross_references><pubmed>32381096</pubmed><doi>10.1186/s12929-020-00656-9</doi></cross_references></HashMap>