Background: Previous studies have shown that sepsis induces systemic inflammation, affecting liver function. Additionally, noise exposure, as an environmental stressor, can exacerbate inflammation and contribute to organ damage. However, the combined effects of noise exposure and sepsis on liver injury have not been extensively studied. This study aimed to investigate the impact of exposure to different noise intensities on lipopolysaccharide (LPS)-induced liver damage in septic rats.

Methods: Healthy 6–8-week-old Wistar rats were randomly assigned to five groups: control, LPS, noise exposure (NE)-45, NE-75, and NE-105, with 20 rats per group. Rats in the experimental groups received intraperitoneal injection of LPS (5 mg/kg) to induce sepsis, followed by exposure to noise at 0, 45, 75, or 105 dB for 1 hour daily over 7 consecutive days. Within 24 hours after the final noise exposure, blood samples were collected for the assessment of liver function-related biochemical parameters. The expression levels of inflammatory factors and related proteins in liver tissue were determined using Enzyme-Linked Immunosorbent Assay (ELISA) and western blot assays. The liver weight/body weight ratio was calculated for each group to evaluate relative changes in liver mass.

Results: Compared to the LPS group, the survival rate of rats in the NE-105 group was significantly reduced to 5–10% (p < 0.01). Serum and liver biochemical tests showed significant increases in alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, as well as in the liver weight/body weight ratio (p < 0.01). Activities of superoxide dismutase (SOD) and glutathione (GSH) were significantly decreased (p < 0.01), while malondialdehyde (MDA) levels were significantly elevated (p < 0.01). ELISA and western blot analyses indicated significant increases in tumor necrosis factor-α (TNF-α) and interleukin 1β (IL-1β) levels in both serum and liver tissue of rats in the NE-105 group (p < 0.01), accompanied by significant upregulation of Toll-like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88), and phosphorylated nuclear factor kappa-light-chain-enhancer of activated B cells p65 (p-NF-κB p65) protein levels (p < 0.01).

Conclusions: High-intensity noise may exacerbate inflammatory responses and oxidative stress in septic rats through the activation of the TLR4/MyD88/NF-κB signaling pathway, thereby significantly aggravating liver damage.