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

Objectives: 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).

Methods: The mouse model with myocardial ischaemic injury was prepared by the left anterior descending coronary artery-amputation and then treated using baicalin.

AhR expression and polymorphisms are associated with risk of coronary arterial disease in Chinese population.

The aryl hydrocarbon receptor (AhR) mediates the control of environmental toxicity, and modulates the development and pathogenesis of the cardiovascular system. However, little is known about the role of AhR in coronary arterial disease (CAD) susceptibility. We therefore conducted a case-control study in a Chinese population, and assessed the potential association between AhR variants and CAD susceptibility.

Baicalin attenuates transforming growth factor-β1-induced human pulmonary artery smooth muscle cell proliferation and phenotypic switch by inhibiting hypoxia inducible factor-1α and aryl hydrocarbon receptor expression.

Objectives: Baicalin, a natural flavone, has antithrombotic, antihyperlipidemic and antiinflammortory activity. It can also inhibit cancer cell proliferation and reduce brain cell apoptosis. This study aimed to elucidate the effect of baicalin on the excessive proliferation of human pulmonary arterial smooth muscle cells (HPASMCs) induced by transforming growth factor-β1 (TGF-β1) and to investigate the roles of hypoxia inducible factor-1α (HIF-1α) and aryl hydrocarbon receptor (AhR) in mediating this TGF-β1-induced excessive proliferation of HPASMCs.