文献类型： 外文期刊

作者： Yuan, Sheng-Nan ¹ ; Wang, Mu-xuan ¹ ; Han, Jin-Long ¹ ; Feng, Cai-Yun ¹ ; Wang, Meng ² ; Wang, Min ³ ; Sun, Jin-Yue ¹ ; Li, Ning-yang ⁴ ; Simal-Gandara, Jesus ⁵ ; Liu, Chao ¹ ;

作者机构： 1.Shandong Acad Agr Sci, Inst Agrofood Sci & Technol, Key Lab Agroprod Proc Technol Shandong Prov, Key Lab Novel Food Resources Proc,Minist Agr & Rur, 202 Gongye North Rd, Jinan 250100, Peoples R China

2.Shanxi Funct Food Engn Ctr Co Ltd, Xian 710000, Peoples R China

3.Northwest A&F Univ, Coll Food Sci & Engn, Xianyang 712100, Peoples R China

4.Shandong Agr Univ, Coll Food Sci & Engn, Key Lab Food Proc Technol & Qual Control Shandong, Tai An, Peoples R China

5.Univ Vigo, Fac Sci, Analyt Chem & Food Sci Dept, Nutr & Bromatol Grp, E-32004 Orense, Spain

6.Shandong Huatai Nutr & Hlth Ind Technol Res Inst C, Jinan 250100, Peoples R China

关键词： Nervonic acid; Macrophages; Inflammatory factors; Ulcerative colitis; NF-kappa B signaling pathway

期刊名称：PHYTOMEDICINE （ 影响因子：7.9； 五年影响因子：6.8 ）

ISSN： 0944-7113

年卷期： 2023 年 112 卷

页码：

收录情况： SCI

摘要： Background: Nervonic acid (C24:1(Delta 15), 24:1 omega-9, cis-tetracos-15-enoic acid; NA), a long-chain monounsaturated fatty acid, plays an essential role in prevention of metabolic diseases, and immune regulation, and has anti-inflammatory properties. As a chronic, immune-mediated inflammatory disease, ulcerative colitis (UC) can affect the large intestine. The influences of NA on UC are largely unknown. Purpose: The present study aimed to decipher the anti-UC effect of NA in the mouse colitis model. Specifically, we wanted to explore whether NA can regulate the levels of inflammatory factors in RAW264.7 cells and mouse colitis model. Methods: To address the above issues, the RAW264.7 cell inflammation model was established by lipopolysaccharide (LPS), then the inflammatory factors tumor necrosis factor-alpha (TNF-alpha), Interleukin-6 (IL-6), Interleukin-1 beta (IL-1 beta), and Interleukin-10 (IL-10) were detected by Enzyme-linked immunosorbent assay (ELISA). The therapeutic effects of NA for UC were evaluated using C57BL/6 mice gavaged dextran sodium sulfate (DSS). Hematoxylin and eosin (H&E) staining, Myeloperoxidase (MPO) kit assay, ELISA, immunofluorescence assay, and LC-MS/MS were used to assess histological changes, MPO levels, inflammatory factors release, expression and distribution of intestinal tight junction (TJ) protein ZO-1, and metabolic pathways, respectively. The levels of proteins involved in the nuclear factor kappa-B (NF-kappa B) pathway in the UC were investigated by western blotting and RT-qPCR. Results: In vitro experiments verified that NA could reduce inflammatory response and inhibit the activation of key signal pathways associated with inflammation in LPS-induced RAW264.7 cells. Further, results from the mouse colitis model suggested that NA could restore intestinal barrier function and suppress NF-kappa B signal pathways to ameliorate DSS-induced colitis. In addition, untargeted metabolomics analysis of NA protection against UC found that NA protected mice from colitis by regulating citrate cycle, amino acid metabolism, pyrimidine and purine metabolism. Conclusion: These results suggested that NA could ameliorate the secretion of inflammatory factors, suppress the NF-kappa B signaling pathway, and protect the integrity of colon tissue, thereby having a novel role in prevention or treatment therapy for UC. This work for the first time indicated that NA might be a potential functional food ingredient for preventing and treating inflammatory bowel disease (IBD).