Lin Ziwei, Zhou Yanlong, Chen Ruiwen, Tao Qiuyan, Lu Qiwen, Xu Qianchao, Yu Haibin, Jiang Ping, Zhao Zhihui
The Key Laboratory of Animal Genetic Resource and Breeding Innovation, College of Coastal Agricultural Sciences, Guangdong Ocean University, Zhanjiang 524088, China.
The Key Laboratory of Animal Resources and Breed Innovation in Western Guangdong Province, Zhanjiang 524088, China.
Mar Drugs. 2025 Jan 9;23(1):31. doi: 10.3390/md23010031.
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.
壳寡糖(COS)作为一种饲料添加剂在动物生产中受到越来越多的关注。COS具有多种生物学功能,包括抗炎和抗氧化活性。乳腺炎是奶牛的一种主要疾病,对动物福利和生产有重大影响。因此,本研究旨在探讨COS对脂多糖(LPS)刺激的牛乳腺上皮细胞(BMECs)炎症反应和氧化应激的作用机制。在本研究中,结果表明COS通过抑制Toll样受体4(TLR4)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β)的过量产生,保护BMECs免受LPS诱导的炎症反应。在LPS诱导的氧化应激条件下,COS处理还抑制了过量活性氧(ROS)的产生并恢复了抗氧化酶活性。此外,结果还表明,COS促进核因子红细胞2相关因子2(Nrf2)的表达,并抑制暴露于LPS的BMECs中TLR4水平以及p65和IκBα的磷酸化。总之,结果表明COS对LPS诱导的炎症反应和氧化应激的保护机制依赖于TLR4/核因子-κB(NF-κB)和Nrf2信号通路,这表明COS可作为缓解乳腺炎中BMECs的天然保护剂。