ArticleFrontiers in pharmacology2025
Licochalcone D mitigates intracerebral hemorrhage-induced ferroptosis of neurons through COX2 inhibition.
Article in Frontiers in pharmacology, 2025. 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
Objective: This study aims to assess LCD's neuroprotective pharmacological effects against SBI post-ICH and identify its ferroptosis-inhibiting targets. Methods: Animal models of ICH and cellular models of SBI were established. Subsequently, gradient concentrations of LCD were administered at both the animal and cellular/molecular levels. The extent of ICH injury was evaluated using a range of methods, including CCK8 assay, Flow Cytometry, quantification of CAT and MDA, CI staining, Western blot, and HE staining. The SWISS TARGET prediction tool and molecular docking were utilized to confirm LCD's target pathway and its binding site on COX2. Quantification of ferroptosis-executing proteins, BODIPY ROS staining, quantification of PGE2, MDA, and CAT were observed to assess the pharmacological effects, trends in ferroptosis influence, and to elucidate the underlying pathway mechanism. Results: Pretreatment with LCD can improve the state of SBI before the induction of an ICH model. Compound target prediction analysis revealed 102 differentially expressed genes ( Conclusion: LCD pretreatment reduces ferroptosis in neurons and alleviates SBI after ICH by blocking the COX2/PGE2/EP1 pathway. Early LCD use may improve SBI, highlighting its potential as a pharmacological option for ICH outcomes.
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