<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Song T</submitter><funding>National Natural Science Foundation of China</funding><pagination>8217035</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11986256</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2025</volume><pubmed_abstract>&lt;b>Background:&lt;/b> Diabetes can cause an increase in intracellular glucose, leading to neuronal damage and microvascular dysfunction. Neuroprotective agents 1&lt;i>α&lt;/i>,25-dihydroxyvitamin D3 (1,25-D3) can reduce neurological complications. The main purpose of this study is to evaluate the levels of inflammatory factors and vascular protective factors in streptozotocin (STZ)-induced diabetic rats and determine whether 1,25-D3 can protect the rat brains from hyperglycemia through the glucagon-like peptide-1 (GLP-1)R/PI3K/AKT signal pathway. &lt;b>Methods:&lt;/b> We first evaluated whether the relevant target could effectively bind to 1,25-D3 through molecular docking. Next, we established STZ-induced diabetic rat models for in vivo experiments to verify the targets in molecular docking that have go</pubmed_abstract><journal>Mediators of inflammation</journal><pubmed_title>1,25-D3 Protects Diabetic Brain Injury Through GLP-1R/PI3K/Akt Pathway by Experimental and Molecular Docking Studies.</pubmed_title><pmcid>PMC11986256</pmcid><funding_grant_id>81870943</funding_grant_id><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Wang B</pubmed_authors><pubmed_authors>Song T</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Zhao Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>1,25-D3 Protects Diabetic Brain Injury Through GLP-1R/PI3K/Akt Pathway by Experimental and Molecular Docking Studies.</name><description>&lt;b>Background:&lt;/b> Diabetes can cause an increase in intracellular glucose, leading to neuronal damage and microvascular dysfunction. Neuroprotective agents 1&lt;i>α&lt;/i>,25-dihydroxyvitamin D3 (1,25-D3) can reduce neurological complications. The main purpose of this study is to evaluate the levels of inflammatory factors and vascular protective factors in streptozotocin (STZ)-induced diabetic rats and determine whether 1,25-D3 can protect the rat brains from hyperglycemia through the glucagon-like peptide-1 (GLP-1)R/PI3K/AKT signal pathway. &lt;b>Methods:&lt;/b> We first evaluated whether the relevant target could effectively bind to 1,25-D3 through molecular docking. Next, we established STZ-induced diabetic rat models for in vivo experiments to verify the targets in molecular docking that have go</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-06-01T10:43:01.373Z</modification><creation>2025-07-14T03:02:45.537Z</creation></dates><accession>S-EPMC11986256</accession><cross_references><pubmed>40224490</pubmed><doi>10.1155/mi/8217035</doi></cross_references></HashMap>