NLRP3 inflammasome inhibition attenuates liver injury and dysfunction induced by noise exposure in rats

• Noise exposure induces glucose and lipid metabolism disorders, liver inflammation and liver damage in rats. • Noise exposure activates the NLRP3 inflammasome in liver cells. • Pharmacological inhibition of NLRP3 inflammasome attenuates noise-induced liver damage and dysfunction. Noise, a significant environmental stressor, has been demonstrated to induce dysregulated glucose and lipid metabolism. However, the precise molecular mechanisms driving liver dysfunction in noise-induced dysregulated glucose and lipid metabolism remain incompletely elucidated. Recent studies have underscored the pivotal role of the NLRP3 (Nod-like receptor protein 3) inflammasome in the context of liver pathology. To this end, a noise-exposure rat model was established (100 dB, 4 hours/day for 30 days) to investigate whether the NLRP3 inflammasome mediates noise-caused hepatic injury and dysfunction. Exposure to noise resulted in significant alterations to liver architecture and dysfunction in rats. Furthermore, we found that noise triggered assembly and activation of the NLRP3 inflammasome, effects that were suppressed by the NLRP3 inhibitor MCC950. Such inbhition thereby attenuated liver damage and improved hepatic function. In conclusion, our findings indicate that noise-induced NLRP3 inflammasome activation promotes hepatic inflammation, contributing to liver injury and dysregulation of glucose and lipid metabolism. These results provide new mechanistic insights into the pathogenesis of noise-induced liver damage and dysfunction. Activation of the NLRP3 inflammasome represents a significant pathological mechanism contributing to the onset of noise-induced liver injury and dysfunction in rats, necessitating two consecutive phases: priming and assembly activation.