期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 15, 期 11, 页码 19355-19368出版社
MDPI
DOI: 10.3390/ijms151119355
关键词
emodin; acute lung injury (ALI); acute respiratory distress syndrome (ARDS); lipopolysaccharide (LPS); E-selectin; MCP-1; nuclear factor-kappa B (NF-kappa B)
资金
- China Postdoctoral Science Foundation [2014M552369]
- National Natural Science Foundation of China [81230001]
- Applying Fundamental Research Foundation of Sichuan Provence of China [2013JY0032]
Acute lung injury (ALI) and its severe manifestation of acute respiratory distress syndrome (ARDS) are well-known illnesses. Uncontrolled and self-amplified pulmonary inflammation lies at the center of the pathology of this disease. Emodin, the bio-active coxund of herb Radix rhizoma Rhei, shows potent anti-inflammatory properties through inactivation of nuclear factor-kappa B (NF-kappa B). The aim of this study was to evaluate the effect of emodin on lipopolysaccharide (LPS)-induced ALI in mice, and its potential bio-mechanism. In our study, BALB/c mice were stimulated with LPS to induce ALI. After 72 h of LPS stimulation, pulmonary pathological changes, lung injury scores, pulmonary edema, myeloperoxidase (MPO) activity, total cells, neutrophils, macrophages, TNF-alpha, IL-6 and IL-1 beta in bronchoalveolar lavage fluid (BALF), and MCP-1 and E-selectin expression were notably attenuated by emodin in mice. Meanwhile, our data also revealed that emodin significantly inhibited the LPS-enhanced the phosphorylation of NF-kappa B p65 and NF-kappa B p65 DNA binding activity in lung. Our data indicates that emodin potently inhibits LPS-induced pulmonary inflammation, pulmonary edema and MCP-1 and E-selectin expression, and that these effects were very likely mediated by inactivation of NF-kappa B in mice. These results suggest a therapeutic potential of emodin as an anti-inflammatory agent for ALI/ARDS treatment.
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