Protective effect of esculentoside A on lipopolysaccharide-induced acute lung injury in mice

被引:49
|
作者
Zhong, Wei-ting [1 ]
Jiang, Lan-xiang [2 ]
Wei, Jing-yuan [1 ,3 ]
Qiao, An-na [1 ]
Wei, Miao-miao [1 ]
Soromou, Lanan-Wassy [1 ,4 ]
Xie, Xian-xing [1 ]
Zhou, Xuan [1 ]
Ci, Xin-xin [1 ]
Wang, Da-cheng [1 ]
机构
[1] Jilin Univ, Key Lab Zoonosis, Minist Educ, Inst Zoonosis,Coll Vet Med, Changchun 130062, Jilin, Peoples R China
[2] Jilin Univ, Hosp 2, Dept Dermatol, Changchun 130062, Jilin, Peoples R China
[3] Liaoning Prov Acad Analyt Sci, Mol Biol Res Lab, Shenyang, Peoples R China
[4] Inst Super Sci & Med Vet ISSMV Dalaba, Dept Vet Med, Dalaba, Guinea
基金
国家高技术研究发展计划(863计划);
关键词
Esculentoside A; Acute lung injury; LPS; MAPK; I kappa Ba; TUMOR-NECROSIS-FACTOR; KAPPA-B; INFLAMMATORY MEDIATORS; MEDICAL PROGRESS; TNF-ALPHA; ENDOTOXIN; RATS; PATHOPHYSIOLOGY; INTERLEUKIN-1; INHIBITION;
D O I
10.1016/j.jss.2013.05.018
中图分类号
R61 [外科手术学];
学科分类号
摘要
Background: Esculentoside A (EsA) is a saponin isolated from the Chinese herb Phytolacca esculenta. In our study, we sought to investigate the protective effects of EsA on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Materials and methods: To determine the effects of EsA on the reduction of histopathologic changes in mice with ALI, inflammatory cell count in bronchoalveolar lavage fluid (BALF) and lung wet-to-dry weight ratio were measured in LPS-challenged mice, and lung histopathologic changes observed via paraffin section were assessed. Next, cytokine production induced by LPS in BALF was measured by enzyme-linked immunosorbent assay. To further study the mechanism of EsA protective effects on ALI, I kappa Ba, p38, and extracellular signal receptor-activated kinase pathways were investigated in lung tissue of mice with ALI. Results: In the present investigation, EsA showed marked effects by reducing inflammatory infiltration, thickening of the alveolar wall, and pulmonary congestion. Levels of tumor necrosis factor alpha and interleukin 6 elevated by LPS were significantly decreased in BALF in EsA-pretreated ALI model. Furthermore, EsA significantly suppressed phosphorylation of I kappa Ba, p38, and extracellular signal receptor-activated kinase. Conclusions: Taken together, our results suggest that EsA suppressed inflammatory responses in LPS-induced ALI through inhibition of the nuclear factor kappa B and mitogen activated protein kinase signaling pathways. EsA may be a promising potential preventive agent for ALI treatment. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:364 / 372
页数:9
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