Asiaticoside attenuates lipopolysaccharide-induced acute lung injury via down-regulation of NF-κB signaling pathway

被引:56
|
作者
Qiu, Jiaming [1 ,2 ]
Yu, Lijun [3 ]
Zhang, Xingxing [2 ]
Wu, Qianchao [2 ]
Wang, Di [3 ]
Wang, Xiuzhi [3 ]
Xia, Cheng [1 ]
Feng, Haihua [2 ]
机构
[1] Heilongiang Bayi Agr Univ, Key Lab Anim Med, Daqing, Peoples R China
[2] Jilin Univ, Coll Vet Med, Key Lab Zoonosis, Minist Educ, Changchun 130062, Jilin, Peoples R China
[3] Inner Mongolia Univ Nationalities, Inst Med Chem & Pharmacol, Tongliao 028000, Inner Mongolia, Peoples R China
关键词
Asiaticoside; ALI; LPS; Cytokines; NF-kappa B; RESPIRATORY-DISTRESS SYNDROME; ALVEOLAR FLUID CLEARANCE; ACTIVATED RAW264.7 CELLS; EPITHELIAL-CELLS; SEPTIC SHOCK; CYTOKINES; SEPSIS; MACROPHAGES; INHIBITION; EXPRESSION;
D O I
10.1016/j.intimp.2015.03.022
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Asiaticoside (AS), a triterpene glycoside isolated from Centella asiatica, has been shown to possess potent anti-inflammatory activity. However, the detailed molecular mechanisms of AS on lipopolysaccharide (LPS)-induced acute lung injury (ALI) model in mice are scanty. The purpose of this study was to evaluate the effect of AS on LPS-induced mouse ALL via down-regulation of NF-kappa B signaling pathway. We investigated the efficacy of AS on cytokine levels induced by LPS in bronchoalveolar lavage fluid (BALF) and RAW 264.7 cells. The production of cytokine (TNF-alpha and IL-6) was measured by enzyme-linked immunosorbent assay (ELISA). The lung wet-to-dry weight ratios were measured in LPS-challenged mice, and lung histopathologic changes observed via paraffin section were assessed. To further study the mechanism of AS protective effects on ALI, the activation of NF-kappa B p65 subunit and the degradation of I kappa B alpha were tested by western blot assay. We found that AS treatment at 15,30 or 45 mg/kg dose-dependently attenuated LPS-induced pulmonary inflammation by reducing inflammatory infiltration, histopathological changes, descended cytokine production, and pulmonary edema initiated by LPS. Furthermore, our results suggested that AS suppressed inflammatory responses in LPS-induced ALI through inhibition of the phosphorylation of NF-kappa B p65 subunit and the degradation of its inhibitor I kappa B alpha, and might be a new preventive agent of ALI in the clinical setting. (c) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:181 / 187
页数:7
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