Elaidic acid-induced intestinal barrier damage led to gut-liver axis derangement and triggered NLRP3 inflammasome in the liver of SD rats
Previous studies have shown that trans fatty acids (TFA) are associated with several chronic diseases, the gut microbiota is directly influenced by dietary components and linked to chronic diseases. Our research investigated the effects of elaidic acid (EA), a typical TFA, on the gut microbiota to u...
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| Format: | Article |
| Language: | English |
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Tsinghua University Press
2024-05-01
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| Series: | Food Science and Human Wellness |
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| Online Access: | https://www.sciopen.com/article/10.26599/FSHW.2022.9250107 |
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| author | Hui Liu Xuenan Li Lu Li Yucai Li Haiyang Yan Yong Pang Wenliang Li Yuan Yuan |
| author_facet | Hui Liu Xuenan Li Lu Li Yucai Li Haiyang Yan Yong Pang Wenliang Li Yuan Yuan |
| author_sort | Hui Liu |
| collection | DOAJ |
| description | Previous studies have shown that trans fatty acids (TFA) are associated with several chronic diseases, the gut microbiota is directly influenced by dietary components and linked to chronic diseases. Our research investigated the effects of elaidic acid (EA), a typical TFA, on the gut microbiota to understand the underlying mechanisms of TFA-related chronic diseases. 16S rDNA gene sequencing on faecal samples from Sprague-Dawley rats were performed to explore the composition change of the gut microbiota by EA gavage for 4 weeks. The results showed that the intake of EA increased the abundance of well-documented harmful bacteria, such as Proteobacteria, Anaerotruncus, Oscillibacter and Desulfovibrionaceae. Plus, EA induced translocation of lipopolysaccharides (LPS) and the above pathogenic bacteria, disrupted the intestinal barrier, led to gut-liver axis derangement and TLR4 pathway activation in the liver. Overall, EA induced intestinal barrier damage and regulated TLR4-MyD88-NF-κB/MAPK pathways in the liver of SD rats, leading to the activation of NLRP3 inflammasome and inflammatory liver damage. |
| format | Article |
| id | doaj-art-979711bed22c43ca9304e9179e0ce71a |
| institution | Kabale University |
| issn | 2097-0765 2213-4530 |
| language | English |
| publishDate | 2024-05-01 |
| publisher | Tsinghua University Press |
| record_format | Article |
| series | Food Science and Human Wellness |
| spelling | doaj-art-979711bed22c43ca9304e9179e0ce71a2025-01-10T06:54:23ZengTsinghua University PressFood Science and Human Wellness2097-07652213-45302024-05-011331279129110.26599/FSHW.2022.9250107Elaidic acid-induced intestinal barrier damage led to gut-liver axis derangement and triggered NLRP3 inflammasome in the liver of SD ratsHui Liu0Xuenan Li1Lu Li2Yucai Li3Haiyang Yan4Yong Pang5Wenliang Li6Yuan Yuan7College of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaPrevious studies have shown that trans fatty acids (TFA) are associated with several chronic diseases, the gut microbiota is directly influenced by dietary components and linked to chronic diseases. Our research investigated the effects of elaidic acid (EA), a typical TFA, on the gut microbiota to understand the underlying mechanisms of TFA-related chronic diseases. 16S rDNA gene sequencing on faecal samples from Sprague-Dawley rats were performed to explore the composition change of the gut microbiota by EA gavage for 4 weeks. The results showed that the intake of EA increased the abundance of well-documented harmful bacteria, such as Proteobacteria, Anaerotruncus, Oscillibacter and Desulfovibrionaceae. Plus, EA induced translocation of lipopolysaccharides (LPS) and the above pathogenic bacteria, disrupted the intestinal barrier, led to gut-liver axis derangement and TLR4 pathway activation in the liver. Overall, EA induced intestinal barrier damage and regulated TLR4-MyD88-NF-κB/MAPK pathways in the liver of SD rats, leading to the activation of NLRP3 inflammasome and inflammatory liver damage.https://www.sciopen.com/article/10.26599/FSHW.2022.9250107elaidic acid (ea)gut microbiotaintestinal barriergut-liver axistlr4-myd88-nf-κb/mapk pathwaysnlrp3 inflammasome |
| spellingShingle | Hui Liu Xuenan Li Lu Li Yucai Li Haiyang Yan Yong Pang Wenliang Li Yuan Yuan Elaidic acid-induced intestinal barrier damage led to gut-liver axis derangement and triggered NLRP3 inflammasome in the liver of SD rats Food Science and Human Wellness elaidic acid (ea) gut microbiota intestinal barrier gut-liver axis tlr4-myd88-nf-κb/mapk pathways nlrp3 inflammasome |
| title | Elaidic acid-induced intestinal barrier damage led to gut-liver axis derangement and triggered NLRP3 inflammasome in the liver of SD rats |
| title_full | Elaidic acid-induced intestinal barrier damage led to gut-liver axis derangement and triggered NLRP3 inflammasome in the liver of SD rats |
| title_fullStr | Elaidic acid-induced intestinal barrier damage led to gut-liver axis derangement and triggered NLRP3 inflammasome in the liver of SD rats |
| title_full_unstemmed | Elaidic acid-induced intestinal barrier damage led to gut-liver axis derangement and triggered NLRP3 inflammasome in the liver of SD rats |
| title_short | Elaidic acid-induced intestinal barrier damage led to gut-liver axis derangement and triggered NLRP3 inflammasome in the liver of SD rats |
| title_sort | elaidic acid induced intestinal barrier damage led to gut liver axis derangement and triggered nlrp3 inflammasome in the liver of sd rats |
| topic | elaidic acid (ea) gut microbiota intestinal barrier gut-liver axis tlr4-myd88-nf-κb/mapk pathways nlrp3 inflammasome |
| url | https://www.sciopen.com/article/10.26599/FSHW.2022.9250107 |
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