title: Retinoid protects rats against neutrophil-induced oxidative stress in acute experimental mastitis.
abstract: Activated polymorphonuclear neutrophilic leukocytes (PMN) are able to produce large quantities of bactericidal molecules such as reactive oxygen species (ROS) that are associated with tissue damage in models of inflammatory mastitis. In this study, the putative protective effect of retinoid was evaluated in a lipopolysaccharide (LPS) induced mastitis model in rats. Commencing at 10 d of gestation, retinoid (dissolved in olive oil) or an equal volume of olive oil were administered daily by gavage to pregnant rats until parturition. LPS or pyrogen-free physiological saline were infused into the mammary gland 72 h after parturition. At pre-infusion (defined as 0 h) and at 2, 4, 8, 16 and 24 h post-infusion, six rats from each group were euthanized. Retinoid administration decreased PMN accumulation in mammary alveoli, significantly decreased the level of TNF-alpha in mammary tissues and IL-8 in serum at the different time points. ROS release was significantly increased after LPS infusion and was reduced by retinoid at 16 h PI. Retinoid reduced N-acetyl-beta-D-glucosaminidase (NAGase) activity in both serum and mammary tissue at 8 h PI. Intercellular adhesion molecule 1 (ICAM-1) mRNA expression reached its peak value earlier in retinoid treated rats than in the control group. Overall, the results suggest that activated PMN play an important role in the pathogenesis of acute mastitis and retinoid administration may be an effective tool for protecting mammary tissue against PMN-induced oxidative stress during LPS-induced acute mastitis.
authors.affiliation: College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China. beibei.gu@163.com
authors.forename: Beibei
authors.initials: B
authors.lastname: Gu
authors.forename: Yumin
authors.initials: Y
authors.lastname: Zhu
authors.forename: Wei
authors.initials: W
authors.lastname: Zhu
authors.forename: Jinfeng
authors.initials: J
authors.lastname: Miao
authors.forename: Yu'e
authors.initials: Y
authors.lastname: Deng
authors.forename: Sixiang
authors.initials: S
authors.lastname: Zou
mesh_terms: D000118:Acetylglucosaminidase / Q000037:antagonists & inhibitors; D000208:Acute Disease; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis / Q000187:drug effects; D016209:Interleukin-8 / Q000097:blood; D008070:Lipopolysaccharides / Q000276:immunology; D008321:Mammary Glands, Animal / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008413:Mastitis / Q000276:immunology / Q000517:prevention & control*; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology; D018384:Oxidative Stress / Q000187:drug effects* / Q000276:immunology; D009195:Peroxidase / Q000276:immunology / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000276:immunology / Q000378:metabolism; D012176:Retinoids / Q000494:pharmacology / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
chemical_list: D016209:Interleukin-8; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D012176:Retinoids; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D009195:Peroxidase; D000118:Acetylglucosaminidase