结肠炎
氧化应激
药理学
肝损伤
抗氧化剂
炎症
溃疡性结肠炎
肿瘤坏死因子α
消炎药
化学
肝功能
医学
免疫学
内科学
生物化学
疾病
作者
Jing Wang,Yongqing Du,Zhengyi Wang,Xiuyu Fang,Haowen Sun,Feng Gao,Tingting Shang,Baoming Shi
摘要
Abstract Background Short‐chain fatty acids have been reported to have anti‐inflammatory and antioxidant functions; whether isobutyrate, a short‐chain fatty acid, is protective against liver injury in a dextran sodium sulfate (DSS)‐induced colitis and its molecular mechanism is unknown. In this study, DSS was used to induce a liver injury from a colitis model in piglets, which was expected to prevent and alleviate DSS‐induced liver injury by feeding sodium isobutyrate in advance. Results The results showed that sodium isobutyrate could restore DSS‐induced histopathological changes in the liver, inhibit the activation of the toll‐like receptor 4/myeloid differentiation primary response 88/nuclear factor kappa‐B signaling pathway, and then reduce the DSS‐induced release of pro‐inflammatory cytokines tumor necrosis factor‐ α , interleukin 1 β , and interleukin 6, reducing inflammatory response. Moreover, we found that sodium isobutyrate could play an antioxidant and apoptosis‐reducing role by maintaining reduced mitochondrial function. Conclusion In conclusion, sodium isobutyrate has a preventive and protective effect on liver injury in a DSS‐induced colitis. There is a potential application prospect for it in treating ulcerative‐colitis‐induced liver injuries. © 2024 Society of Chemical Industry.
科研通智能强力驱动
Strongly Powered by AbleSci AI