ArticleMolecular diversity2026
Baicalin attenuates angiotensin II-induced vascular endothelial injury via targeted activation of the Nrf2 signaling pathway: Integrated computational and in vitro evidence.
Article in Molecular diversity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Angiotensin II (AngII)-mediated oxidative stress is a primary driver of vascular endothelial dysfunction, a critical pathogenesis in hypertension and cardiovascular diseases. While baicalin is recognized for its cardioprotective properties, the precise atomic-level mechanism governing its interaction with the Nrf2 signaling axis remains to be fully characterized. This study employs an integrated in silico and in vitro framework to elucidate the molecular determinants by which baicalin mitigates AngII-induced endothelial injury. Quantum chemical calculations using Density Functional Theory (DFT) revealed a relatively narrow HOMO-LUMO energy gap (∆E = 3.86 eV), suggesting enhanced electronic reactivity and a potential tendency toward redox-related activity. Pharmacokinetic profiling further predicted a favorable ADMET profile with negligible toxicity risks. Molecular docking and 500 ns molecular dynamics (MD) simulations identified a stable, high-affinity binding mode (∆G
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