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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 916590, 11 pages
http://dx.doi.org/10.1155/2013/916590
Research Article

Therapeutic Effect of C-Phycocyanin Extracted from Blue Green Algae in a Rat Model of Acute Lung Injury Induced by Lipopolysaccharide

1Department of Intensive Care, Chi Mei Medical Center Liou Ying Campus, Tainan, Taiwan
2Department of Surgery, Chi Mei Medical Center, Liou Ying Campus, Tainan, Taiwan
3Institute of Physiology, National Defense Medical Center, Taipei, Taiwan
4Department of Biomedical Engineering, National Defense Medical Center, Institute of Medical Sciences, Tzu Chi University, 701 Zhongyang Road, Hualien, Taiwan

Received 3 November 2012; Revised 20 February 2013; Accepted 21 February 2013

Academic Editor: Jenny M. Wilkinson

Copyright © 2013 Pak-on Leung et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

C-Phycocyanin (CPC), extracted from blue green algae, is a dietary nutritional supplement due to its several beneficial pharmacological effects. This study was conducted to evaluate whether CPC protects against lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in rats. Rats were challenged with LPS (5 mg/kg body weight) intratracheally to induce ALI. After 3 h LPS instillation, rats were administrated with CPC (50 mg/kg body weight, i.p.) for another 3 h. Our results showed that posttreatment with CPC significantly inhibited LPS-induced elevation of protein concentration, nitrite/nitrate level, release of proinflammatory cytokines, the number of total polymorphonuclear cells in bronchoalveolar lavage fluid, and lung edema evidenced by decrease of lung wet/dry weight ratio accompanied by a remarkable improvement of lung histopathological alterations. Furthermore, CPC significantly attenuated LPS-induced myeloperoxidase activity, formation, expression of inducible nitric oxide synthase, and cyclooxygenase-2 as well as nuclear factor-kappa B (NF-κB) activation in lungs. Additionally, CPC significantly downregulated proapoptotic proteins such as caspase-3 and Bax, but upregulated antiapoptotic proteins such as Bcl-2 and Bcl-XL in lungs exposed to LPS. These findings indicate that CPC could be potentially useful for treatment of LPS-related ALI by inhibiting inflammatory responses and apoptosis in lung tissues.