Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 118, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2019.109217
Keywords
NLRP3 inflammasome; Radiotherapy; Radiation damage; Inflammatory signaling pathway; IL-1 beta; ROS
Funding
- National Natural Science Foundation of China [81570344]
- Norman Bethune Program of Jilin University [2015225, 2015203]
- Jilin Provincial Science and Technology Foundations [20180414039GH, 20190201200JC]
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Radiotherapy (RT) is currently one of the leading treatment for various cancers and it may cause injury to healthy tissue, with both short-term and long-term side effects. Inflammatory responses play an important role in the adverse reactions of early and late ionizing radiation. Nucleotide-binding domain and leucine-rich-repeatcontaining family pyrin 3 (NLRP3) inflammasome as a multi-protein complex that activates caspase-1 can give rise to the proinflammatory cytokines such as interleukin-18 (IL-18) and interleukin-1 beta (IL-1 beta) maturation. Recent experiments and studies have shown that up-regulation of NLRP3 inflammasome have a big impact on radiation damage, which include radiation-induced oral mucositis, radiation-induced skin reactions, radiation-induced lung damage, radiation-induced intestinal injury and radiation-induced changes in other systems. In this paper, we will review the role of NLRP3 inflammasome in radiation damage, to explore possible therapeutic strategies for radiation damage.
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