Dihydromyricetin ameliorates chronic liver injury by reducing pyroptosis

Figure 6 Working model of the pyroptosis-related pathway. CCl₄ treatment stimulates the formation of NOD-, LRR- and pyrin domain-containing 3 inflammasome, which activates caspase-1. While caspase-1 activates interleukin-1β, it cleaves gasdermin D (GSDMD) into the carboxyl terminal (GSDMD-C) and amino terminal (GSDMD-N). GSDMD-N binds to the lipid membrane and polymerizes into an oligomer with a pore in the middle. This channel allows passage of materials < 10 nm in diameter. More pores are formed, which cause cell membrane damage and rupture, and eventually chronic liver injury. DHM: Dihydromyricetin; NLRP3: NOD-, LRR- and pyrin domain-containing 3; IL-1β: Interleukin-1β; GSDMD: Gasdermin D.