Melatonin Inhibits Lipopolysaccharide-Induced Inflammation and Oxidative Stress in Cultured Mouse Mammary Tissue. (12th February 2019)

• Record Type: Journal Article
• Authors: Yu, Guang-Min; Tan, Wen
• Other Names: Hatanaka Elaine Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2019(2019)
• Publication Date: 2019-02-12
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2019/8597159
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : To determine whether melatonin can protect cultured mouse mammary tissue from lipopolysaccharide- (LPS-) induced damage, we investigated the effects of melatonin on the mRNA and protein levels of proinflammatory cytokines and chemokines in LPS-stimulated mammary tissue in vitro . This study also examined the IgG level in both cultured mammary tissue and the culture medium. In addition, we investigated the potential benefits of melatonin on the expression of antioxidant relative genes following LPS treatment in cultured mammary tissue and evaluated ROS level in the culture medium. The results demonstrate that melatonin inhibited the mRNA expression of TNF-α, IL-1β, IL-6, CXCL1, MCP-1, and RANTES and the production of these cytokines and chemokines and IgG in LPS-stimulated mouse mammary tissue in vitro . In addition, melatonin increased Nrf2 but decreased iNOS and COX-2 mRNA expression after LPS stimulation. Similarly, the decreased level of dityrosine in the culture medium was increased by treatment with melatonin, while increased nitrite level was suppressed. This study confirms that melatonin inhibited LPS-induced inflammation and oxidative stress in cultured mouse mammary tissue. It might contribute to mastitis therapy while treating antibiotic resistance.