Protective Effects of Chitosan Oligosaccharide Against Lipopolysaccharide-Induced Inflammatory Response and Oxidative Stress in Bovine Mammary Epithelial Cells

氧化应激 TLR4型 脂多糖 肿瘤坏死因子α 活性氧 化学 抗氧化剂 细胞因子 白细胞介素 药理学 信号转导 免疫学 生物 生物化学
作者
Ziwei Lin,Yanlong Zhou,Ruiwen Chen,Q. T. Tao,Quan Lü,Qiong Xu,Haibin Yu,Ping Jiang,Zhihui Zhao
出处
期刊:Marine Drugs [Multidisciplinary Digital Publishing Institute]
卷期号:23 (1): 31-31 被引量:2
标识
DOI:10.3390/md23010031
摘要

Chitosan oligosaccharide (COS) is receiving increasing attention as a feed additive in animal production. COS has a variety of biological functions, including anti-inflammatory and antioxidant activities. Mastitis is a major disease in dairy cows that has a significant impact on animal welfare and production. Hence, this research aimed to investigate the mechanism of COS on the lipopolysaccharide (LPS)-stimulated inflammatory response and oxidative stress in bovine mammary epithelial cells (BMECs). In this study, the results demonstrated that COS protected BMECs from the inflammatory response induced by LPS by restraining the excessive production of toll-like receptor 4 (TLR4), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). COS treatment also suppressed excessive reactive oxygen species (ROS) production and restored antioxidant enzyme activity under LPS-induced oxidative stress conditions. Furthermore, the results also demonstrated that COS promote nuclear factor erythroid 2-related factor 2 (Nrf2) expression and inhibit TLR4 levels and p65 and IκBα phosphorylation in BMECs exposed to LPS. In summary, the results demonstrate that the protective mechanism of COS on the LPS-induced inflammatory response and oxidative stress depend on the TLR4/nuclear factor-κB (NF-κB) and Nrf2 signaling pathways, indicating that COS could serve as natural protective agents for alleviating BMECs in mastitis.
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