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. 2019 Dec 16;13:553. doi: 10.3389/fncel.2019.00553

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Copyright © 2019 Ye, Jin, Zhang, Zeng, Ye, Wang, Zhong, Xiong and Gu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential mechanisms by which Meisoindigo protects against focal cerebral ischemia-reperfusion injury (CIRI). Activation of the NLRP3 inflammasome and microglia/macrophage polarization strongly influence the immunological cascades triggered by stroke. Meisoindigo reduces the production of inflammatory mediators by inhibiting the activation of the NLRP3 inflammasome and preventing the microglial/macrophage switch from the protective M2 phenotype to the pro-inflammatory M1 phenotype, thereby exerting neuroprotection against ischemic stroke, which may achieve through the inhibition of TLR4/NF-κB signaling pathway in neurons and microglia. In addition, we here found that the NLRP3 inflammasome is mainly expressed in neurons. Therefore, we speculate that the inflammatory mediators released by NLRP3 inflammasome1 activation in neurons may induce neuronal pyroptosis and affect phenotypic polarization in microglia/macrophages.