Title : Fine particulate matter exposure aggravates ischemic injury via NLRP3 inflammasome activation and pyroptosis.

Pub. Date : 2022 Jul

PMID : 35403328






4 Functional Relationships(s)
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1 Finally, the intracellular reactive oxygen species (ROS) was measured and the ROS inhibitor N-acetyl-L-cysteine (NAC) was used to investigate whether ROS was required for PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions. Reactive Oxygen Species NLR family pyrin domain containing 3 Homo sapiens
2 Moreover, we observed that PM2.5 exposure increased the production of intracellular ROS following OGD/R, while inhibiting ROS production with NAC partially attenuated PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions. Reactive Oxygen Species NLR family pyrin domain containing 3 Homo sapiens
3 Moreover, we observed that PM2.5 exposure increased the production of intracellular ROS following OGD/R, while inhibiting ROS production with NAC partially attenuated PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions. Reactive Oxygen Species NLR family pyrin domain containing 3 Homo sapiens
4 CONCLUSION: These results suggested that PM2.5 exposure triggered the activation of NLRP3 inflammasome and pyroptosis under ischemic conditions, which may be mediated by increased ROS production after ischemic stroke. Reactive Oxygen Species NLR family pyrin domain containing 3 Homo sapiens