The
nucleotide-binding oligomerization domain (
NOD)-like receptor (NLR) family pyrin domain-containing 3 (NLRP3)
inflammasome is a member of the NLR family of inherent immune cell sensors. The NLRP3
inflammasome can detect tissue damage and pathogen invasion through innate immune cell sensor components commonly known as
pattern recognition receptors (
PRRs).
PRRs promote activation of
nuclear factor kappa B (NF-κB) pathways and the
mitogen-activated protein kinase (MAPK) pathway, thus increasing the transcription of genes encoding
proteins related to the NLRP3
inflammasome. The NLRP3
inflammasome is a complex with multiple components, including an NAIP, CIITA, HET-E, and TP1 (NACHT) domain; apoptosis-associated speck-like
protein containing a CARD (ASC); and a
leucine-rich repeat (LRR) domain. After
ischemic stroke, the NLRP3
inflammasome can produce numerous proinflammatory
cytokines, mediating nerve cell dysfunction and
brain edema and ultimately leading to nerve cell death once activated.
Ischemic stroke is a disease with high rates of mortality and disability worldwide and is being observed in increasingly younger populations. To date, there are no clearly effective therapeutic strategies for the clinical treatment of
ischemic stroke. Understanding the NLRP3
inflammasome may provide novel ideas and approaches because targeting of upstream and downstream molecules in the NLRP3 pathway shows promise for
ischemic stroke therapy. In this manuscript, we summarize the existing evidence regarding the composition and activation of the NLRP3
inflammasome, the molecules involved in inflammatory pathways, and corresponding drugs or molecules that exert effects after
cerebral ischemia. This evidence may provide possible targets or new strategies for
ischemic stroke therapy.