Comparative analysis of noise and music exposure on inflammatory responses on lipopolysaccharide-induced septic rats

Author:

Liu Hu1,Peng Xing-guo1,Gao Ran1,Yang Kai1,Zhao Yan-bo1ORCID

Affiliation:

1. Department of Emergency and Critical Care Center, Renmin Hospital, Hubei University of Medicine, Hubei, China

Abstract

Objective Environmental factors such as noise and music can significantly impact physiological responses, including inflammation. This study explored how environmental factors like noise and music affect lipopolysaccharide (LPS)-induced inflammation, with a focus on systemic and organ-specific responses. Materials and Methods 24 Wistar rats were divided into four groups ( n = 6 per group): Control group, LPS group, noise-exposed group, and music-exposed group. All rats, except for the Control group, received 10 mg/kg LPS intraperitoneally. The rats in the noise-exposed group were exposed to 95 dB noise, and the music-exposed group listened to Mozart’s K. 448 music (65–75 dB) for 1 h daily over 7 days. An enzyme-linked immunosorbent assay was utilized to detect the levels of inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), in serum and tissues (lung, liver, and kidney). Western blot examined the phosphorylation levels of nuclear factor-κB (NF-κB) p65 in organ tissues. Results Compared with the Control group, LPS-induced sepsis rats displayed a significant increase in the levels of TNF-α and IL-1β in serum, lung, liver, and kidney tissues, as well as a remarkable elevation in the p-NF-κB p65 protein expression in lung, liver, and kidney tissues. Noise exposure further amplified these inflammatory markers, while music exposure reduced them in LPS-induced sepsis rats. Conclusion Noise exposure exacerbates inflammation by activating the NF-κB pathway, leading to the up-regulation of inflammatory markers during sepsis. On the contrary, music exposure inhibits NF-κB signaling, indicating a potential therapeutic effect in reducing inflammation.

Publisher

SAGE Publications

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