文摘
BackgroundRecently, several studies have demonstrated that the NLRP3 inflammasome participates in detecting cellular damage and mediating inflammatory responses to aseptic tissue injury following cerebral ischemia. More importantly, blocking or inhibiting NLRP3 inflammasome at multiple levels, such as its expression, assembly and activity, may offer substantial promise to salvage neurological deterioration during ischemic stroke. However, the specific mechanisms about the contribution of NLRP3 to neurovascular damage remain to be established.