The Ability of Hydroxysafflor Yellow A to Attenuate Lipopolysaccharide-induced Pulmonary Inflammatory Injury in Mice

被引:75
作者
Sun, Chun-Yan [1 ]
Pei, Chong-qiang [1 ]
Zang, Bao-Xia [1 ]
Wang, Lin [1 ]
Jin, Ming [1 ]
机构
[1] Capital Med Univ, Beijing Anzhen Hosp, Beijing Inst Heart Lung & Blood Vessel Dis, Dept Pharmacol, Beijing 100029, Peoples R China
基金
中国国家自然科学基金;
关键词
hydroxysafflor yellow A; lipopolysaccharide; pulmonary inflammatory injury; P38 MAP KINASE; FACTOR-KAPPA-B;
D O I
10.1002/ptr.3166
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Hydroxysafflor yellow A (HSYA) is a component of the flower of Carthamus tinctorius L. The present study investigated whether HSYA could attenuate acute lung injury (ALL) induced by lipopolysaccharide (LPS) administration. Male Kunming mice were pretreated with HSYA 0.5 h prior to intraperitoneal application of LPS. Arterial blood gas, lung water content index, lung tissue myeloperoxidase (M PO) activity, mRNA expression of inflammatory cytokines, NF-kappa Bp65, p38 mitogen-activated protein kinase (MAPK) and pathological changes in lung morphology were assessed. After LPS administration, all animals displayed increased arterial carbon dioxide partial pressure (PaCO2), and decreased arterial oxygen partial pressure (PaO2), arterial oxygen saturation (SO2), HCO3- concentration and pH, which were ameliorated by pretreating the animals with HSYA. HSYA administration significantly attenuated inflammatory cell infiltration and alleviated pulmonary edema induced by LPS. Moreover, HSYA decreased NF-kappa B p65 nuclear translocation, inhibited proinflammatory cytokine TNF-alpha, IL-1 beta and IL-6 mRNA expression and promoted antiinflammatory cytokine IL-10 gene expression following LPS injection. Pulmonary p38 MAPK phosphorylation was upregulated 4 h after LPS treatment, which could be suppressed by pretreatment with HSYA. These findings demonstrated the protective effect of HSYA against LPS-induced acute lung injury, which is suggested to be associated with the inhibition of p38 MAPK, NF-kappa B p65 activation and alteration of inflammatory cytokine expression. Copyright (C) 2010 John Wiley & Sons, Ltd.
引用
收藏
页码:1788 / 1795
页数:8
相关论文
共 25 条
[1]   Nuclear factor-κB and its role in sepsis-associated organ failure [J].
Abraham, E .
JOURNAL OF INFECTIOUS DISEASES, 2003, 187 :S364-S369
[2]   Role of p38 MAP kinase in the development of acute lung injury [J].
Arcaroli, J ;
Yum, HK ;
Kupfner, J ;
Park, JS ;
Yang, KY ;
Abraham, E .
CLINICAL IMMUNOLOGY, 2001, 101 (02) :211-219
[3]   Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome [J].
Bhatia, M ;
Moochhala, S .
JOURNAL OF PATHOLOGY, 2004, 202 (02) :145-156
[4]   The role of nuclear factor-kappa B in cytokine gene regulation [J].
Blackwell, TS ;
Christman, JW .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1997, 17 (01) :3-9
[5]   Acute respiratory distress syndrome: update on the latest developments in basic and clinical research [J].
Bosma, Karen ;
Fanelli, Vito ;
Ranieri, V. Marco .
CURRENT OPINION IN ANESTHESIOLOGY, 2005, 18 (02) :137-145
[6]   Nonventilatory treatments for acute lung injury and ARDS [J].
Calfee, Carolyn S. ;
Matthay, Michael A. .
CHEST, 2007, 131 (03) :913-920
[7]  
Chen Ting-ting, 2008, Yaoxue Xuebao, V43, P570
[8]   Transcriptional mechanisms of acute lung injury [J].
Fan, J ;
Ye, RD ;
Malik, AB .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2001, 281 (05) :L1037-L1050
[9]   Caveolin-1 regulates NF-κB activation and lung inflammatory response to sepsis induced by lipopolysaccharide [J].
Garrean, Sean ;
Gao, Xiao-Pei ;
Brovkovych, Victor ;
Shimizu, Jun ;
Zhao, You-Yang ;
Vogel, Stephen M. ;
Malik, Asrar B. .
JOURNAL OF IMMUNOLOGY, 2006, 177 (07) :4853-4860
[10]   Local stimulation of α7 cholinergic receptors inhibits LPS-induced TNF-α release in the mouse lung [J].
Giebelen, Ida A. J. ;
van Westerloo, David J. ;
LaRosa, Gregory J. ;
de Vos, Alex F. ;
van der Poll, Tom .
SHOCK, 2007, 28 (06) :700-703