Mounting evidence has demonstrated that NLRP3 inflammasome plays a prominent role in the pathogenesis and progression of ischemic stroke, which indicates the higher possibility to target NLRP3 inflammasome in future stroke therapy. However, many aspects of the biology of NLRP3 inflammasome to stroke are still not well defined or even completely unknown. As the mechanistic insight of the NLRP3 inflammasomes increases, opportunities to develop new therapeutic strategies for patients with ischemic stroke are expected to enhance proportionately.

: Ischemic stroke is one of the main causes of mortality and disability worldwide. However, the efficient therapeutic strategies are still lacking. Stem/progenitor cell-based therapy, with its vigorous advantages, has emerged as a promising tool for the treatments of ischemic stroke. The mechanisms involve new neural cells and neuronal circuitry formation, antioxidation, inflammation alleviation, angiogenesis and neurogenesis promotion. In the past decades, in-depth studies have suggested that cell therapy could promote vascular stabilization and decrease blood-brain barrier (BBB) leakage after ischemic stroke. However, the effects and underlying mechanisms on BBB integrity induced by the engrafted cells in ischemic stroke have not been reviewed yet. Herein, we will update the progress in researches of the effects of cell therapy on BBB integrity after ischemic stroke and review the underlying mechanisms. First, we will present an overview of BBB dysfunction under ischemic condition and cells engraftment for ischemic treatment. Then we will summarize and discuss the current knowledge about the effects and underlying mechanisms of cell therapy on BBB integrity after ischemic stroke. In particular, we will review the most recent studies in regard to the relationship between cell therapy and BBB in tissue plasminogen activator (t-PA)-mediated therapy and diabetic stroke.