Dataset Information

The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.

ABSTRACT: The increasing risk of long-term adverse effects from radiotherapy on the cardiovascular structure is receiving increasing attention. However, the mechanisms underlying this increased risk remain poorly understood. Recently, the nucleotide-binding domain and leucine-rich-repeat-containing family pyrin 3 (NLRP3) inflammasome was suggested to play a critical role in radiation-induced cardiovascular injury. However, the relationship between ionizing radiation and the NLRP3 inflammasome in acute and chronic inflammation is complex. We reviewed literature detailing pathological changes and molecular mechanisms associated with radiation-induced damage to the cardiovascular structure, with a specific focus on NLRP3 inflammasome-related cardiovascular diseases. We also summarized possible therapeutic strategies for the prevention of radiation-induced heart disease (RIHD).

SUBMITTER: Huang S

PROVIDER: S-EPMC7080656 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.

Huang Shanshan S Che Jing J Chu Qian Q Zhang Peng P

Frontiers in cell and developmental biology 20200312

The increasing risk of long-term adverse effects from radiotherapy on the cardiovascular structure is receiving increasing attention. However, the mechanisms underlying this increased risk remain poorly understood. Recently, the nucleotide-binding domain and leucine-rich-repeat-containing family pyrin 3 (NLRP3) inflammasome was suggested to play a critical role in radiation-induced cardiovascular injury. However, the relationship between ionizing radiation and the NLRP3 inflammasome in acute and ...[more]

PMID: 32226786

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Project description:BackgroundVentilator-induced lung injury (VILI) is caused by stretch stimulation and other factors related to mechanical ventilation (MV). NOD-like receptor protein 3 (NLRP3), an important innate immune component, is strongly associated with VILI. This study aimed to investigate the effect and mechanisms of aerobic exercise (EX) on VILI.MethodsTo test the effects of the PKC inhibitor bisindolylmaleimide I on PKC and NLRP3, male C57BL/6 mice (7 weeks old, 19 ~ 23 g) were randomly divided into four groups: control group(C), bisindolylmaleimide I-pretreated group(B), MV group, and bisindolylmaleimide I-pretreated + MV (B + MV) group. The mice were pretreated with bisindolylmaleimide I through intraperitoneal injection (0.02 mg/kg) 1 h before MV. MV was performed at a high tidal volume (30 ml/kg). To explore the ameliorative effect of EX on VILI, the mice were randomly divided into C group, MV group, EX group and EX + MV group and subjected to either MV or 5 weeks of EX training. After ventilation, haematoxylin-eosin (HE) staining and wet/dry weight ratio was used to assess lung pathophysiological changes. PKCɑ, P-PKCɑ, ASC, procaspase-1, caspase-1, pro-IL-1β, IL-1β, NLRP3 and occludin (tight junction protein) expression in lung tissues was determined by Western blotting. The level of IL-6 in alveolar lavage fluid was determined by ELISA.ResultsNLRP3, P-PKCɑ, and PKCɑ levels were inceased in MV group, but bisindolylmaleimide I treatment reversed these changes. Inhibition of PKC production prevented NLRP3 activation. Moreover, MV increased ASC, procaspase-1, caspase-1, pro-IL-1β, and IL1β levels and decreased occludin levels, but EX alleviated these changes. HE staining and lung injury scoring confirmed an absence of obvious lung injury in C group and EX group. Lung injury was most severe in MV group but was improved in EX + MV group. Overall, these findings suggest that MV activates the NLRP3 inflammasome by activating PKCɑ and inducing occludin degradation, while Exercise attenuates NLRP3 inflammasome and PKCɑ activation. Besides, exercise improves cyclic stretch-induced degradation of occludin.ConclusionPKC activation can increase the level of NLRP3, which can lead to lung injury. Exercise can reduce lung injury by inhibiting PKCɑ and NLRP3 activation. Exercise maybe a potential measure for clinical prevention of VILI.

Dataset Information

The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.

Publications

The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.

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