Protective Effect of Magnolol on Lipopolysaccharide-Induced Acute Lung Injury in Mice
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Protective Effect of Magnolol on Lipopolysaccharide-Induced Acute Lung Injury in Mice Yun Feng Ni,1 Tao Jiang,1 Qing Shu Cheng,1 Zhong Ping Gu,1 Yi Fang Zhu,1 Zhi Pei Zhang,1 Jian Wang,1 Xiao Long Yan,1 Wu Ping Wang,1 Chang Kang Ke,1 Yong Han,1,2 and Xiao Fei Li1,2
Abstract—Magnolol, a tradition Chinese herb, displays an array of activities including antifungal, antibacterial, and antioxidant effects. To investigate the protective effect of magnolol on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. ALI was induced in mice by intratracheal instillation of LPS (1 mg/kg). The mice received intratracheal instillation of magnolol (5 μg/kg) 30 min before LPS administration. Pulmonary histological changes were evaluated by hematoxylineosin stain and lung wet/dry weight ratios were observed. Concentrations of tumor necrosis factor (TNF)-α and interleukin (IL)-1β, and myeloperoxidase (MPO) activity were measured by enzymelinked immunosorbent assay. Expression of cyclooxygenase (COX)-2 in lung tissues was determined by Western blot analysis. Magnolol pretreatment significantly attenuated the severity of lung injury and inhibited the production of TNF-α and IL-1β in mice with ALI. After LPS administration, the lung wet/dry weight ratios, as an index of lung edema, and MPO activity were also markedly reduced by magnolol pretreatment. The expression of COX-2 was significantly suppressed by magnolol pretreatment. Magnolol potently protected against LPS-induced ALI and the protective effects of magnolol may attribute partly to the suppression of COX-2 expression. KEY WORDS: lipopolysaccharide; acute lung injury; magnolol; cyclooxygenase-2; tumor necrosis factor-α; interleukin-1β.
INTRODUCTION Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), represent a clinical syndrome that results from complex responses of the lung to a multitude of direct and indirect insults [1]. Although the causes of ALI and ARDS are numerous, endotoxin is thought to be the most pathogen that leads to the development of ALI and ARDS. Endotoxin or lipopolysacchride (LPS), derived from the cell wall of gram-negative bacteria, induces a sepsis syndrome accompanied by key features of ALI, including the Yun Feng Ni and Tao Jiang authors contributed equally to this work and should be regarded as co-first authors. 1
Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi’an, 710038, China 2 To whom correspondence should be addressed at Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi’an, 710038, China. E-mail: [email protected]; E-mail: [email protected]
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2012 Springer Science+Business Media, LLC
recruitment of inflammatory cells into the lung with subsequent increases in capillary permeability and alveolar edema [2]. Despite improvement in intensive care, ALI/ARDS have mortality rates of 40–70 % [3]. Cyclooxygenase (COX) catalyses the committed step in the metabolism of arachidonic acid
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