Figure 3.

TLR4/NLRP3 signaling pathway inhibition by acylated-ghrelin to reduce I/R-induced cardiomyocyte infarction and inflammation. During myocardial I/R injury, TLR4 is expressed on the surface of the myocardial cell membrane, and PAMPs and DAMPs bind to it to release ROS. ROS activates NLRP3 inflammasome, which in turn promotes the activation of procaspase-1 to caspase-1. Caspase-1 promotes the release of inflammatory factors IL-1β and IL-18 from the cell and triggers the inflammatory response. Ghrelin can downregulate the expression of TLR4, thereby inhibiting the occurrence of the inflammatory response and alleviating myocardial injury caused by I/R. TLR4, Toll-like receptor 4; PAMPs, Pathogen-associated molecular patterns; DAMPs, damage associated molecular patterns; ROS, reactive oxygen species; NLRP3, NOD-like receptor thermal protein domain associated protein 3; IL-1β&IL-18, interleukin 1β&interleukin 18. Created with BioRender.com.