system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Acute Lung Injury, Animals, Anti-Infective Agents, Cytokines, Disease Models, Animal, Female, Humans, Lipopolysaccharides, Lung, Mice, Mice, Inbred BALB C, Nitric Oxide, Shock, Septic, Treatment Outcome, Triterpenes.
user
Does ursolic acid attenuate lipopolysaccharide-induced acute lung injury in a mouse model? Context: To assess whether ursolic acid (UA) can attenuate lipopolysachharide (LPS)-induced acute lung injury and improve the survival time in a mouse model. 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. 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.
assistant
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. Final Decision: yes