S/O/W Emulsion with CAPE Ameliorates DSS-Induced Colitis by Regulating NF-κB Pathway, Gut Microbiota and Fecal Metabolome in C57BL/6 Mice.
Xuelin WeiJuan DaiRuijia LiuGuochao WanShiyu GuYuwei DuXinyue YangLijun WangYukun HuangPengfei ChenXianggui ChenXiao YangQin WangPublished in: Nutrients (2024)
Inflammatory bowel disease (IBD) has attracted much attention worldwide due to its prevalence. In this study, the effect of a solid-in-oil-in-water (S/O/W) emulsion with Caffeic acid phenethyl ester (CAPE, a polyphenolic active ingredient in propolis) on dextran sulfate sodium (DSS)-induced colitis in C57BL/6 mice was evaluated. The results showed that CAPE-emulsion could significantly alleviate DSS-induced colitis through its effects on colon length, reduction in the disease activity index (DAI), and colon histopathology. The results of ELISA and Western blot analysis showed that CAPE-emulsion can down-regulate the excessive inflammatory cytokines in colon tissue and inhibit the expression of p65 in the NF-κB pathway. Furthermore, CAPE-emulsion promoted short-chain fatty acids production in DSS-induced colitis mice. High-throughput sequencing results revealed that CAPE-emulsion regulates the imbalance of gut microbiota by enhancing diversity, restoring the abundance of beneficial bacteria (such as Odoribacter ), and suppressing the abundance of harmful bacteria (such as Afipia , Sphingomonas ). The results of fecal metabolome showed that CAPE-emulsion restored the DSS-induced metabolic disorder by affecting metabolic pathways related to inflammation and cholesterol metabolism. These research results provide a scientific basis for the use of CPAE-emulsions for the development of functional foods for treating IBD.
Keyphrases
- south africa
- disease activity
- signaling pathway
- oxidative stress
- rheumatoid arthritis
- fatty acid
- systemic lupus erythematosus
- high fat diet induced
- poor prognosis
- lps induced
- high throughput sequencing
- type diabetes
- ulcerative colitis
- binding protein
- risk factors
- high glucose
- juvenile idiopathic arthritis
- nuclear factor
- physical activity
- skeletal muscle
- long non coding rna