Formononetin Inhibited the Inflammation of LPS-Induced Acute Lung Injury in Mice Associated with Induction of PPAR Gamma
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Formononetin Inhibited the Inflammation of LPS-Induced Acute Lung Injury in Mice Associated with Induction of PPAR Gamma Expression Zhanqiang Ma,1 Weiwei Ji,1 Qiang Fu,1,2 and Shiping Ma1,2
Abstract—Formononetin has shown a variety of pharmacologic properties including anti-inflammatory effect. In the present study, we analyzed the role of formononetin in acute lung injury induced by lipopolysaccharide (LPS) in mice. The cell counting in the bronchoalveolar lavage fluid (BALF) was measured. The animal lung edema degree was evaluated by wet/dry weight ratio. The superoxidase dismutase (SOD) activity and myeloperoxidase (MPO) activity was assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, tumor necrosis factor-α (TNF-α) and IL-6,were assayed by enzyme-linked immunosorbent assay method. Pathological changes of hung tissues were observed by HE staining. Peroxisome proliferator-activated receptor (PPAR)-γ gene expression was measured by real-time PCR. The data showed that treatment with the formononetin group markedly attenuated inflammatory cell numbers in the BALF, increased PPAR-γ gene expression and improved SOD activity and inhibited MPO activity. The histological changes of the lungs were also significantly improved by formononetin compared to LPS group. The results indicated that formononetin has a protective effect on LPS-induced acute lung injury in mice. KEY WORDS: formononetin; inflammation; PPAR-γ; LPS-induced acute lung injury.
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 main pathogen that leads to the development of ALI and ARDS. Endotoxin or lipopolysaccharide (LPS), derived from the cell wall of gram-negative bacteria, induces a sepsis syndrome accompanied by key features of ALI, including the recruitment of inflammatory cells into the lung with subsequent increases in capillary permeability and alveolar edema [2]. It is often shown as hypoxemia, alveolar–capillary barrier
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Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, Jiangsu 210009, People’s Republic of China 2 To whom correspondence should be addressed at Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, Jiangsu 210009, People’s Republic of China. E-mail: [email protected]; [email protected]
1560 0360-3997/13/0600-1560/0
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2013 Springer Science+Business Media New York
damage, and pulmonary inflammation, and is associated with multiple organ failure in later stage. There is no specific medicine to control ALI or ARDS as yet, so searching for the new therapy target and exploring the new drug to treat ARDS has become the important work of scientific research. Animal models of ALI are important tools for studying mechanisms relevant to th
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