Biochanin A inhibits endothelial dysfunction induced by IL‑6‑stimulated endothelial microparticles in Perthes disease via the NFκB pathway

Endothelial dysfunction caused by the stimulation of endothelial microparticles (EMPs) by the inflammatory factor IL‑6 is one of the pathogenic pathways associated with Perthes disease. The natural active product biochanin A (BCA) has an anti‑inflammatory effect; however, whether it can alleviate endothelial dysfunction in Perthes disease is not known. The present in vitro experiments on human umbilical vein endothelial cells showed that 0‑100 pg/ml IL‑6‑EMPs could induce endothelial dysfunction in a concentration‑dependent manner, and the results of the Cell Counting Kit 8 assay revealed that, at concentrations of <20 µM, BCA had no cytotoxic effect. Reverse transcription‑quantitative PCR demonstrated that BCA reduced the expression levels of the endothelial dysfunction indexes E‑selectin and intercellular cell adhesion molecule‑1 (ICAM‑1) in a concentration‑dependent manner. Immunofluorescence and western blotting illustrated that BCA increased the expression levels of zonula occludens‑1 and decreased those of ICAM‑1. Mechanistic studies showed that BCA inhibited activation of the NFκB pathway. In vivo experiments demonstrated that IL‑6 was significantly increased in the rat model of ischemic necrosis of the femoral head, whereas BCA inhibited IL‑6 production. Therefore, in Perthes disease, BCA may inhibit the NFκB pathway to suppress IL‑6‑EMP‑induced endothelial dysfunction, and could thus be regarded as a potential treatment for Perthes disease.