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. 2022 Sep 27;13:926895. doi: 10.3389/fimmu.2022.926895

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Copyright © 2022 Ghafouri-Fard, Shoorei, Poornajaf, Hussen, Hajiesmaeili, Abak, Taheri and Eghbali

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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A schematic illustration of the role of NLRP3 Inflammasome and its central role in the myocardial I/R injury. Accumulating evidence has illustrated that Luteolin could have a key role in protecting against myocardial I/R injury as opposed to Uric acid that could aggravate this injury through ROS/NLRP3 pyroptosis pathway. It has been reported that Luteolin could protect against myocardial I/R injury through TLR4/NF-kB/NLRP3 inflammasome cascade by downregulating the expressions of NLRP3, ASC, caspase-1, TLR4, MyD88 and the phosphorylations of IKKα, IKKβ, IκBα, and NF-κB (71).