Chrysophanol Inhibits NALP3 Inflammasome Activation and Ameliorates Cerebral Ischemia/Reperfusion in Mice

Figure 1

Model of danger signals activation of the NALP3 inflammasome. Tissue injury leads to the formation and release of danger signals such as ATP or uric acid crystals that are recognized by the innate immune system. A number of these signals mediate a potassium efflux or other secondary intracellular danger signals that are required for NALP3 inflammasome activation [51, 52]. NALP3 inflammasome then oligomerizes to recruit the adaptor ASC and caspase-1 [53]. Activation of caspase-1 results in the processing and maturation of pro IL-1β into its biologically active form, active IL-1β [12, 54]. Active IL-1β will then trigger the IL-1β receptor, leading to the activation of multiple cytokines involved in the inflammation cascade [55].