Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 12, Issue 1, Pages 88-93Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2011.10.018
Keywords
Ruscogenin; Lipopolysaccharide (LPS); Acute lung injury (ALI); Tissue factor (TF); Inducible NO synthase (iNOS); Nuclear factor (NF)-kappa B
Categories
Funding
- National Natural Science Foundation of China [90713042]
- Program for New Century Excellent Talents in University [NCET-07-0849]
- National Foundation for Fostering Talents of Basic Sciences [NFFTBS-J0630858]
- Priority Academic Program Development of Jiangsu Higher Education Institutions
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Acute lung injury is still a significant clinical problem with a high mortality rate and there are few effective therapies in clinic. Here, we studied the inhibitory effect of ruscogenin, an anti-inflammatory and antithrombotic natural product, on lipopolysaccharide (LPS)-induced acute lung injury in mice basing on our previous studies. The results showed that a single oral administration of ruscogenin significantly decreased lung wet to dry weight (W/D) ratio at doses of 0.3, 1.0 and 3.0 mg/kg 1 h prior to LPS challenge (30 mg/kg, intravenous injection). Histopathological changes such as pulmonary edema, coagulation and infiltration of inflammatory cells were also attenuated by ruscogenin. In addition, ruscogenin markedly decreased LPS-induced myeloperoxidase (MPO) activity and nitrate/nitrite content, and also downregulated expression of tissue factor (IF), inducible NO synthase (iNOS) and nuclear factor (NF)-kappa B p-p65 (Ser 536) in the lung tissue at three doses. Furthermore, ruscogenin reduced plasma TF procoagulant activity and nitrate/nitrite content in LPS-induced ALI mice. These findings confirmed that ruscogenin significantly attenuate LPS-induced acute lung injury via inhibiting expressions of TF and iNOS and NF-kappa B p65 activation, indicating it as a potential therapeutic agent for ALI or sepsis. (C) 2011 Elsevier B.V. All rights reserved.
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