Baicalin inhibits inflammation and attenuates myocardial ischaemic injury by aryl hydrocarbon receptor

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Recent evidence indicates that suppressing inflammation by specific drug target and treatment measures contributes to attenuate ischaemic injury and the related heart diseases. This study aimed to investigate the potential effect of baicalin on myocardial ischaemic injury through inhibition of inflammation by inactivating the aryl hydrocarbon receptor (AhR).


The mouse model with myocardial ischaemic injury was prepared by the left anterior descending coronary artery-amputation and then treated using baicalin. After observing the expression of AhR by immunohistochemical staining, the AhR and inflammatory mediators in circulation and myocardial tissues, including high-sensitive C-reactive protein (hsCRP), interleukin (IL)-1β and IL-6, were detected based on enzyme-linked immunosorbent assay, real-time polymerase chain reaction and Western blot methods.

Key findings

The results showed that (1) substantial expression of AhR was observed in myocardial tissues; (2) ischaemic injury caused myocardial necrosis and remodelling, and stimulated hsCRP, IL-1β and IL-6 by activation of AhR; and (3) baicalin alleviated the myocardial injury and inflammatory response by inhibiting the expression of AhR.


Our findings extend the list of AhR ligands beyond exogenous toxins and endogenous molecules to cardiac immunological factors, and moreover it could be considered potential drug targets due to its pathological modulatory properties, while baicalin demonstrated promise as a novel vehicle for ischaemic heart disease.

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