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Pulmonary function changes in rats with taurocholate-induced pancreatitis are attenuated by pretreatment with melatonin

Authors

  • Ting-Ywan Chou,

    1. Medical Imaging Department, Cardinal Tien Hospital, New Taipei City, Taiwan
    2. School of Medicine, College of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan
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  • Russel J. Reiter,

    1. Department of Cellular & Structural Biology, The University of Texas Health Science Center, San Antonio, TX, USA
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  • Kuan-Hao Chen,

    1. Jen-Teh Junior College of Medicine and Nursing Management, Miaoli, Taiwan
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  • Fur-Jiang Leu,

    1. School of Medicine, College of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan
    2. Department of Pathology, Cardinal Tien Hospital, New Taipei City, Taiwan
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  • David Wang,

    1. School of Medicine, College of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan
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  • Diana Y. Yeh

    Corresponding author
    1. School of Medicine, College of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan
    2. Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
    • Address reprint requests to Diana Yuwung Yeh, Division of Chest Medicine, Department of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, 95 WenChang Rd., Taipei 11101, Taiwan.

      E-mail: dyyeh@yahoo.com

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Abstract

Melatonin is a free radical scavenger and broad-spectrum antioxidant with immunomodulatory effects. We studied the effects of melatonin on changes in lung function, oxidative/nitrosative stress, and inflammatory cell sequestration in an acute pancreatitis (AP)-associated lung inflammation model. Acute pancreatitis was induced by injection of 5% sodium taurocholate into the pancreatic duct of rats. Animals were randomized into control, AP, and a melatonin pretreatment (10 mg/kg)/AP group. Functional residual capacity (FRC), lung compliance (Cchord), expiratory flow rate at 50% (FEF50), airway resistance index (RI), and peak expiratory flow rate (PEF) were evaluated. White blood cell count (WBC) and hydrogen peroxide, lung lavage fluid WBC, methylguanidine, protein, lactic dehydrogenase (LDH), nitric oxide (NO), and leukotriene B4 (LTB4) levels were determined. Lung wet-to-dry weight ratio, peroxynitrite, and inducible nitric oxide synthase (NOS) mRNA and protein were measured. AP induction resulted in reductions in FRC, Cchord, FEF50, and PEF, and increase in RI and lung wet-to-dry weight ratio. Blood and lung lavage fluid WBC, lavage fluid LDH, protein, and blood hydrogen peroxide also increased. Levels of hydroxyl radicals, nitric oxide, and LTB4 in lung lavage fluid, inducible NOS mRNA, protein expression, and peroxynitrite in lung tissue also were significantly elevated. Pretreatment with melatonin attenuated obstructive and restrictive ventilatory insufficiency induced by AP. Blood and lavage WBC, lavage LDH and protein, lung edema, oxidative/nitrosative stress, and lipoxygenase pathway derivatives were also significantly attenuated by melatonin. We conclude that melatonin decreases AP-induced obstructive and restrictive lung function changes via its antioxidant and anti-inflammatory properties.

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