Ganoderic acid B attenuates LPS-induced lung injury

Area of Science:

• Pharmacology
• Immunology
• Respiratory Medicine

Background:

• Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) presents a significant clinical challenge with unclear underlying mechanisms.
• Lipopolysaccharide (LPS) is a common inducer of pneumonia and acute lung injury models.

Purpose of the Study:

• To elucidate the protective mechanism of ganoderic acid B (BB) in a mouse model of LPS-induced pneumonia.
• To investigate the role of the Rho/NF-κB signaling pathway in the therapeutic effects of BB.

Main Methods:

• A pneumonia model was established using LPS in mice and A549 cells.
• Evaluated lung injury markers including dry/wet weight ratio (W/D) and myeloperoxidase (MPO) activity.
• Assessed histopathological changes via HE staining, oxidative stress markers (SOD, MDA), and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6).
• Examined Rho/NF-κB pathway activation using Western Blot.

Main Results:

• BB treatment significantly reduced lung W/D ratio and MPO activity, ameliorating lung histopathology.
• BB increased superoxide dismutase (SOD) levels and decreased malondialdehyde (MDA), TNF-α, IL-1β, and IL-6.
• BB effectively inhibited the activation of the Rho/NF-κB pathway in both mice and A549 cells.

Conclusions:

• Ganoderic acid B (BB) demonstrates a protective effect against LPS-induced pneumonia in mice.
• The therapeutic mechanism of BB is associated with the modulation of the Rho/NF-κB signaling pathway, reducing inflammation and oxidative stress.