Magnolol Mitigates Lung Injury in Sepsis Mice by Reducing Inflammatory Response and Oxidative Stress and Regulating HMGB1/TLR4/NF-κB Signaling Pathway

The objective of this study was to investigate the mitigating effect of magnolol on lung injury in sepsis mice and the mechanisms. Fifty mice were randomly divided into sham-operated, sepsis and 5, 10, and 20 mg/kg magnolol groups, 10 mice in each group. The sepsis model was prepared in sepsis and 5, 10, and 20 mg/kg magnolol groups by cecal ligation and perforation. Before 30 min from modeling, the 5, 10, and 20 mg/kg magnolol groups were intraperitoneally injected with 5, 10, and 20 mg/kg magnolol, respectively. After 24 h from modeling, the blood gas indexes, lung injury indexes, inflammatory response, and oxidative stress indexes and High-Mobility Group Box 1 (HMGB1)/Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-kappa B) signaling pathway were determined. Results showed that, compared with sepsis group, in 10 and 20 mg/kg magnolol groups the partial pressure of oxygen and oxygenation index significantly increased, and the lung wet-dry weight ratio and lung tissue myeloperoxidase activity significantly decreased, the lung tissue tumor necrosis factor alpha, IL-1 beta, and IL-6 levels significantly decreased, the lung tissue superoxide dismutase and glutathione peroxidase levels significantly increased, the lung tissue malondialdehyde and xanthine oxidase levels significantly decreased, and the lung tissue HMGB1, TLR4 and NF-kappa B protein expression levels significantly decreased. Magnolol can mitigate the lung injury in sepsis mice. The mechanisms may be related to its reduction of inflammatory response and oxidative stress and down-regulation of HMGB1/TLR4/NF-kappa B signaling pathway.