Conclusions
By blocking the IRAK1/TAK1 pathway, AF can significantly slow the course of AS, suggesting that it could be a viable therapeutic option for AS.
Results
Our results verified that AF could not only dramatically accelerate viability and cholesterol efflux but also attenuate inflammation, ROS production, and apoptosis in Ox-LDL-induced HUVECs. Meanwhile, AF could prominently prevent the activation of IRAK1-TAK1 pathway, downregulate apoptosis-related proteins, and upregulate mitochondrial fusion-related proteins in Ox-LDL-induced HUVECs. Moreover, we testified that IRAK1 overexpression memorably could reverse suppression of AF on inflammation, apoptosis, and IRAK1-TAK1 pathway and enhancement of AF on viability, cholesterol efflux, and mitochondrial fusion in Ox-LDL-induced HUVECs. Conclusions: By blocking the IRAK1/TAK1 pathway, AF can significantly slow the course of AS, suggesting that it could be a viable therapeutic option for AS.