Xiangjun Chen1, Yang Wan, Taoyou Zhou, Jiong Li, Yuquan Wei. 1. State 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.
Abstract
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.
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.