Research progress about the role of NLRP3 in ischemic stroke

Ischemic stroke is the second leading cause of death worldwide and a major cause of permanent disability.Inflammasomes play a key role in the post-stroke inflammation.NLRP3 is currently the most characterized inflammasome.After stroke, the release of DAMPs from necrotic cells in the ischemic core and the changes of intracellular microenvironment trigger the formation of inflammasome, activating caspase-1 and mediating the secretion of IL-1β and IL-18, ultimately leading to cell death through inflammatory and /or apoptotic processes.Researches showed that minocycline, sinomenine, iris and intravenous immunoglobulin could inhibit the expression of NLRP3 after cerebral ischemia/reperfusion injury, and then control the cell injury caused by inflammation.Further exploration on the inflammatory response induced by NLRP3 and related mechanisms can promote the clinical application of anti-inflammatory treatment to ischemic stroke. Key words: Ischemic stroke; Inflammasome; NLRP3