Seabuckthorn Paste Protects Lipopolysaccharide-Induced Acute Lung Injury in Mice through Attenuation of Oxidative Stress

被引：17

作者：

Du, Leilei ^{[1
,2
]}

Hu, Xiaoxin ^{[1
]}

Chen, Chu ^{[3
]}

Kuang, Tingting ^{[1
]}

Yin, Hengfu ^{[1
]}

Wan, Li ^{[2
]}

机构：

[1] Chengdu Univ Tradit Chinese Med, Coll Ethnomed, Chengdu, Sichuan, Peoples R China

[2] Chengdu Univ Tradit Chinese Med, Coll Pharm, Chengdu, Sichuan, Peoples R China

[3] Sichuan Acad Chinese Med Sci, Chengdu, Sichuan, Peoples R China

来源：

OXIDATIVE MEDICINE AND CELLULAR LONGEVITY | 2017年 / 2017卷

基金：

中国国家自然科学基金;

关键词：

HIGH-ALTITUDE; ANTIOXIDANT; PERMEABILITY;

D O I：

10.1155/2017/4130967

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Oxidative stress is one of the major mechanisms implicated in endotoxin-induced acute lung injury. Seabuckthorn paste (SP), a traditional Tibetan medicine with high content of polyphenols and remarkable antioxidant activity, is commonly used in treating pulmonary diseases. In the present study, the protective effects and possible underlying mechanisms of SP on lipopolysaccharide- (LPS-) induced acute lung injury in mice were investigated. It was found that body weight loss, lung tissue microstructure lesions, transvascular leakage increase, malondialdehyde augmentation, and the reduction of superoxide dismutase and glutathione peroxidase levels caused by LPS challenge were all consistently relieved by SP treatment in a dose-dependent manner. Moreover, accumulation of nuclear factor erythroid 2-related factor 2 (Nrf2) in lung nuclei caused by SP treatment was observed. Our study demonstrated that SP can provide significant protection against LPS-induced acute lung injury through maintaining redox homeostasis, and its mechanism involves Nrf2 nuclear translocation and activation.

引用

页数：9

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