Abstract
The development of next generation therapy for ischemic stroke is important for the aging society. To control post-ischemic inflammation could be a hopeful therapeutic approach. In this review, we focus on the triggers of inflammation after ischemic stroke. Various danger associated molecular patterns (DAMPs) activate pattern recognition receptors (PRRs) in immune cells and trigger the acute sterile inflammation in brain. The activation of inflammasome is also important for IL-1β production in ischemic brain. Ibrutinib can be a therapeutic agent for ischemic stroke by inhibiting the activity of Bruton’s tyrosine kinase (BTK) which promotes the inf lammasome activation. Thus, further investigation of inflammatory mechanisms will develop a novel therapeutic strategy for ischemic stroke.
