{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Song T"],"funding":["National Natural Science Foundation of China"],"pagination":["8217035"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11986256"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["2025"],"pubmed_abstract":["<b>Background:</b> Diabetes can cause an increase in intracellular glucose, leading to neuronal damage and microvascular dysfunction. Neuroprotective agents 1<i>α</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. <b>Methods:</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"],"journal":["Mediators of inflammation"],"pubmed_title":["1,25-D3 Protects Diabetic Brain Injury Through GLP-1R/PI3K/Akt Pathway by Experimental and Molecular Docking Studies."],"pmcid":["PMC11986256"],"funding_grant_id":["81870943"],"pubmed_authors":["Li X","Li Y","Li J","Wang B","Song T","Wang Y","Zhao Y"],"additional_accession":[]},"is_claimable":false,"name":"1,25-D3 Protects Diabetic Brain Injury Through GLP-1R/PI3K/Akt Pathway by Experimental and Molecular Docking Studies.","description":"<b>Background:</b> Diabetes can cause an increase in intracellular glucose, leading to neuronal damage and microvascular dysfunction. Neuroprotective agents 1<i>α</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. <b>Methods:</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","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-06-01T10:43:01.373Z","creation":"2025-07-14T03:02:45.537Z"},"accession":"S-EPMC11986256","cross_references":{"pubmed":["40224490"],"doi":["10.1155/mi/8217035"]}}