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

Exp Ther Med. 2024 Feb 13;27(4):137. doi: 10.3892/etm.2024.12425. eCollection 2024 Apr.ABSTRACTEndothelial 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...

Source: Experimental and Therapeutic Medicine - March 13, 2024 Category: General Medicine Authors: Jianhong Liu Chengsen Lin Boxiang Li Qian Huang Xianxiang Chen Shengping Tang Xiaolin Luo Rongbin Lu Yun Liu Shijie Liao Xiaofei Ding Source Type: research