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Inhibition of NLRP3 inflammasome attenuates spinal cord injury‐induced lung injury in mice
Author(s) -
Jiang Wu,
Li Maoqiang,
He Fan,
Zhu Liulong
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27233
Subject(s) - inflammasome , spinal cord injury , spinal cord , lung , medicine , spinal injury , anesthesia , pharmacology , inflammation , immunology , psychiatry
Spinal cord injury (SCI) is one kind of severe traumatic injury, resulting in systemic inflammatory response syndrome and secondary lung injury, which is an important pathological basis of respiratory complications. The nucleotide‐binding domain‐like receptor protein 3 (NLRP3) inflammasome is an important cytosolic protein complex in many inflammatory diseases. Hence, it is inescapable to explore the effect of inhibition of NLRP3 inflammasome by inhibitors in a mouse SCI model, which was conducted by using the method of 30‐G closing force aneurysm clipping at T6–T7 spinal segment for 1 min, followed by assessment of edema, histology, alveolar type II cell apoptosis, mitochondrial dysfunction, and neutrophil infiltration. In brief, our results showed that, NLRP3 inflammasome inhibitor BAY 11‐7082 or A438079 inhibited activation of NLRP3 inflammasome, alleviated mitochondrial dysfunction, the number of macrophage and neutrophil, thereby attenuating alveolar type II cell apoptosis, lung edema, and histological injury. Taken together, our data reveal that NLRP3 inflammasome inhibitor BAY 11‐7082 or A438079 attenuates the inflammatory response, reverses mitochondrial dysfunction, and subsequently alleviates secondary lung injury following SCI.