Prolonged exposure to a music-enriched environment mitigates acute noise-induced inflammation and apoptosis in the chicken spleen by modulating the Keap-1/Nrf2 and NF-κB pathways.

ABSTRACT

The rise of operational noise as an environmental pollutant for farm animals is an emerging concern. The mechanisms through which music can alleviate oxidative stress, inflammation, and apoptosis induced by noise exposure remain underexplored. This study aims to investigate the alleviating effects and underlying mechanisms of long-term music exposure on noise-induced damage to the chicken spleen. Male Arbor Acres (AA) broilers were divided into four groups control (C), acute noise stimulation (NS), noise stimulation with music mitigation (NSM), and music only (M). NS and NSM groups were exposed to noise (simulating sudden intensity noise, 115 to 120dB) for 10 minutes daily for a week, starting at 14-days-old. NSM and M groups then received 28 days of 6-hour daily music (Mozart K.448, 60-65 dB). The results showed that noise stimulation significantly activated the Keap-1/Nrf2 and NF-κB signaling pathways. Long-term music intervention has also been demonstrated to successfully mitigate oxidative stress and abnormal apoptosis induced by acute noise stimulation. Microscopic examination of the spleen revealed that acute noise stimulation resulted in an increase in splenic cells, a decrease in lymphocytes, and blurred boundaries between the red and white pulps in the NS group. However, these pathological changes were alleviated in the NSM group following music intervention. Compared with the control group, the NS group exhibited significantly elevated oxidative stress parameters. In contrast, music intervention in the NSM group notably improved antioxidant capacity and partially alleviated morphological abnormalities in the spleen. Additionally, noise stimulation activated the NF-κB pathway, upregulating the downstream genes of the inflammatory factors IL-1ß, IL-6, and TNF-α. Noise-induced mitochondrial damage led to apoptosis, as observed by TUNEL staining, along with increased gene and protein expression of Bcl-2, Bax, Cyt-C, Casp-3, Casp-8, and Casp-9. These findings indicate that acute noise exposure can induce splenic damage via oxidative stress, inflammation, and apoptosis by modulating the Keap-1/Nrf2 and NF-κB pathways. Prolonged music stimulation effectively mitigates noise-induced damage, offering a vital experimental foundation for further research on noise pollution's impact on organisms and music's alleviating role.