1,25-D3 Protects Diabetic Brain Injury Through GLP-1R/PI3K/Akt Pathway by Experimental and Molecular Docking Studies.

ABSTRACT: Background: Diabetes can cause an increase in intracellular glucose, leading to neuronal damage and microvascular dysfunction. Neuroprotective agents 1α,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. Methods: 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

SUBMITTER: Song T 

PROVIDER: S-EPMC11986256 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature