Effects of salidroside on atherosclerosis: potential contribution of gut microbiota

Abstract

Graphical AbstractThis review seeks to offer a comprehensive look at how salidroside impacts gut microbiota and its potential therapeutic role in treating atherosclerosis. (A) Salidroside has been shown to have a positive impact on atherosclerosis by promoting the growth of beneficial bacteria and decreasing the levels of harmful bacteria in the body. (B) Salidroside has been shown to enhance the integrity and function of the intestinal mucosal barrier through its ability to suppress NF-κB and p38 MAPK signaling pathways, modulate the NF-κB/MAPK/JAK-STAT3 signaling pathways and increase the expression of antimicrobial peptides HD-5 and HD-6. (C) Salidroside can reduce TMAO production through reducing the abundance of Firmicutes and Proteobacteria. (D) Salidroside can improve the expression of SCFAs, through increasing the abundance of some special bacteria. (E) Salidroside can reduce LPS-induced inflammation, which is associated with the inhibition of the ROS-mediated PI3K/AKT/mTOR signaling pathway, the downregulation of exosome miR-199a-5p, and the attenuation of the Notch-Hes signaling pathway. (F) Salidroside can inhibit NLRP3-associated gut-coronary axis, including TLR4/MyD88/NF-κB/NLRP3 signaling pathway, AMPK/NF-κB/NLRP3 signaling pathway, and P2X7/NF-κB/NLRP3 signaling pathway.