Ursolic acid attenuates lipopolysaccharide-induced acute lung injury in a mouse model

被引：7
作者：
Chen, Xiangjun [1 ]
Wan, Yang [1 ]
Zhou, Taoyou [2 ,3 ]
Li, Jiong [4 ,5 ]
Wei, Yuquan [1 ]
机构：
[1] Sichuan Univ, State Key Lab Biotherapy, West China Hosp, West China Med Sch, Chengdu 610041, Peoples R China
[2] Sichuan Univ, Dept Infect Dis, West China Hosp 2, Chengdu 610041, Peoples R China
[3] Sichuan Univ, West China Med Sch, West China Hosp, Chengdu 610041, Peoples R China
[4] Sichuan Univ, State Key Lab Biotherapy, West China Hosp, Chengdu 610041, Peoples R China
[5] Sichuan Univ, Sch Life Sci, Chengdu 610041, Peoples R China
来源：
IMMUNOTHERAPY | 2013年 / 5卷 / 01期
关键词：
acute lung injury; cytokine; LPS; sepsis; ursolic acid; NF-KAPPA-B; PROINFLAMMATORY CYTOKINE; INFLAMMATORY RESPONSE; SEPSIS; HMGB1; NEUTROPHILS; EXPRESSION;
D O I：
10.2217/IMT.12.144
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
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-alpha, IL-6, IL-1 beta, 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-kappa B, 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-alpha, IL-6, IL-10, 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-kappa B, 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.
引用
收藏
页码：39 / 47
页数：9
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