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Updated: May 15, 2026
Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Ursolic acid attenuates lipopolysaccharide-induced acute lung injury in a mouse model
Xiangjun Chen1, Yang Wan, Taoyou Zhou
1State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, 1# Keyuan Road 4, Gao-peng Street, High Technological Development Zone, Chengdu, 610041, PR China.
Aim:
To assess whether ursolic acid (UA) can attenuate lipopolysachharide (LPS)-induced acute lung injury and improve the survival time in a mouse model.
Materials & Methods:
The mice were challenged with LPS and survival time was monitored from 0-96 h after LPS treatment. TNF-α, IL-6, IL-1β, HMGB1, nitric oxide (NO) and IL-10 concentration in serum were measured by ELISA. Myeloperoxidase activity, malondialdehyde, lung wet:dry weight ratio and lung permeability in lung tissues were detected. NF-κB, HMGB1 and inducible NO synthase in the lungs were detected by western blot.
Results:
UA markedly rescued lethality, improved survival time and lung pathological changes, inhibited TNF-α, IL-6, IL-1β, HMGB1 and NO, and increased IL-10 expression. In addition, UA can also decrease myeloperoxidase, malondialdehyde, lung wet:dry weight ratio and lung permeability. UA attenuated NF-κB, HMGB1 and inducible NO synthase protein expression in the lungs.
Conclusion:
The results suggest that UA is capable of improving survival time and LPS-induced acute lung injury. UA has a potentially therapeutic role in septic shock.
