Protective Effect and Mechanisms of Eckol on Chronic Ulcerative Colitis Induced by Dextran Sulfate Sodium in Mice
The use of functional foods and their bioactive components is receiving increasing attention as a complementary and alternative therapy for chronic ulcerative colitis (UC). This study explored the protective effect and mechanisms of Eckol, a seaweed-derived bioactive phlorotannin, on the dextran sod...
Main Authors: | , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2023-06-01
|
Series: | Marine Drugs |
Subjects: | |
Online Access: | https://www.mdpi.com/1660-3397/21/7/376 |
_version_ | 1797588521671720960 |
---|---|
author | Mengfan Liao Songyi Wei Xianmin Hu Juan Liu Jun Wang |
author_facet | Mengfan Liao Songyi Wei Xianmin Hu Juan Liu Jun Wang |
author_sort | Mengfan Liao |
collection | DOAJ |
description | The use of functional foods and their bioactive components is receiving increasing attention as a complementary and alternative therapy for chronic ulcerative colitis (UC). This study explored the protective effect and mechanisms of Eckol, a seaweed-derived bioactive phlorotannin, on the dextran sodium sulfate (DSS)-induced chronic UC in mice. Eckol (0.5–1.0 mg/kg) reduced DSS-enhanced disease activity indexes, and alleviated the shortening of colon length and colonic tissue damage in chronic UC mice. The contents of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 were significantly decreased, and the level of anti-inflammatory IL-10 was enhanced in the serum and colonic tissues collected from Eckol-treated mice compared with the DSS controls. Eckol administration significantly reduced the number of apoptotic cells and the expression of cleaved Caspase-3, and increased the B-cell lymphoma-2 (Bcl-2)/B-cell lymphoma-2- associated X (Bax) ratio in DSS-challenged colons. There were more cluster of differentiation (CD)11c<sup>+</sup> dendritic cells and CD8<sup>+</sup> T cells, and less CD4<sup>+</sup> T cells infiltrated to inflamed colonic tissues in the Eckol-treated groups. Expression of colonic Toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB) p65, phosphorylated-signal transducer and activator of transcription (pSTAT)3 was significantly down-regulated by Eckol compared with the DSS-challenged group. In conclusion, our data suggest that Eckol appeared to be a potential functional food ingredient for protection against chronic UC. The anti-colitis mechanisms of Eckol might be attributed to the down-regulation of the TLR4/NF-κB/STAT3 pathway, inhibition of inflammation and apoptosis, as well as its immunoregulatory activity. |
first_indexed | 2024-03-11T00:54:13Z |
format | Article |
id | doaj.art-d1411e5e346b480a9ff29a3967b143b2 |
institution | Directory Open Access Journal |
issn | 1660-3397 |
language | English |
last_indexed | 2024-03-11T00:54:13Z |
publishDate | 2023-06-01 |
publisher | MDPI AG |
record_format | Article |
series | Marine Drugs |
spelling | doaj.art-d1411e5e346b480a9ff29a3967b143b22023-11-18T20:13:55ZengMDPI AGMarine Drugs1660-33972023-06-0121737610.3390/md21070376Protective Effect and Mechanisms of Eckol on Chronic Ulcerative Colitis Induced by Dextran Sulfate Sodium in MiceMengfan Liao0Songyi Wei1Xianmin Hu2Juan Liu3Jun Wang4Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Institute of Pharmaceutical Innovation, School of Medicine, Wuhan University of Science and Technology, Wuhan 430065, ChinaHubei Province Key Laboratory of Occupational Hazard Identification and Control, Institute of Pharmaceutical Innovation, School of Medicine, Wuhan University of Science and Technology, Wuhan 430065, ChinaHubei Province Key Laboratory of Occupational Hazard Identification and Control, Institute of Pharmaceutical Innovation, School of Medicine, Wuhan University of Science and Technology, Wuhan 430065, ChinaHubei Province Key Laboratory of Occupational Hazard Identification and Control, Institute of Pharmaceutical Innovation, School of Medicine, Wuhan University of Science and Technology, Wuhan 430065, ChinaHubei Province Key Laboratory of Occupational Hazard Identification and Control, Institute of Pharmaceutical Innovation, School of Medicine, Wuhan University of Science and Technology, Wuhan 430065, ChinaThe use of functional foods and their bioactive components is receiving increasing attention as a complementary and alternative therapy for chronic ulcerative colitis (UC). This study explored the protective effect and mechanisms of Eckol, a seaweed-derived bioactive phlorotannin, on the dextran sodium sulfate (DSS)-induced chronic UC in mice. Eckol (0.5–1.0 mg/kg) reduced DSS-enhanced disease activity indexes, and alleviated the shortening of colon length and colonic tissue damage in chronic UC mice. The contents of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 were significantly decreased, and the level of anti-inflammatory IL-10 was enhanced in the serum and colonic tissues collected from Eckol-treated mice compared with the DSS controls. Eckol administration significantly reduced the number of apoptotic cells and the expression of cleaved Caspase-3, and increased the B-cell lymphoma-2 (Bcl-2)/B-cell lymphoma-2- associated X (Bax) ratio in DSS-challenged colons. There were more cluster of differentiation (CD)11c<sup>+</sup> dendritic cells and CD8<sup>+</sup> T cells, and less CD4<sup>+</sup> T cells infiltrated to inflamed colonic tissues in the Eckol-treated groups. Expression of colonic Toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB) p65, phosphorylated-signal transducer and activator of transcription (pSTAT)3 was significantly down-regulated by Eckol compared with the DSS-challenged group. In conclusion, our data suggest that Eckol appeared to be a potential functional food ingredient for protection against chronic UC. The anti-colitis mechanisms of Eckol might be attributed to the down-regulation of the TLR4/NF-κB/STAT3 pathway, inhibition of inflammation and apoptosis, as well as its immunoregulatory activity.https://www.mdpi.com/1660-3397/21/7/376Eckolchronic ulcerative colitisinflammationapoptosisimmunoregulationTLR4 pathway |
spellingShingle | Mengfan Liao Songyi Wei Xianmin Hu Juan Liu Jun Wang Protective Effect and Mechanisms of Eckol on Chronic Ulcerative Colitis Induced by Dextran Sulfate Sodium in Mice Marine Drugs Eckol chronic ulcerative colitis inflammation apoptosis immunoregulation TLR4 pathway |
title | Protective Effect and Mechanisms of Eckol on Chronic Ulcerative Colitis Induced by Dextran Sulfate Sodium in Mice |
title_full | Protective Effect and Mechanisms of Eckol on Chronic Ulcerative Colitis Induced by Dextran Sulfate Sodium in Mice |
title_fullStr | Protective Effect and Mechanisms of Eckol on Chronic Ulcerative Colitis Induced by Dextran Sulfate Sodium in Mice |
title_full_unstemmed | Protective Effect and Mechanisms of Eckol on Chronic Ulcerative Colitis Induced by Dextran Sulfate Sodium in Mice |
title_short | Protective Effect and Mechanisms of Eckol on Chronic Ulcerative Colitis Induced by Dextran Sulfate Sodium in Mice |
title_sort | protective effect and mechanisms of eckol on chronic ulcerative colitis induced by dextran sulfate sodium in mice |
topic | Eckol chronic ulcerative colitis inflammation apoptosis immunoregulation TLR4 pathway |
url | https://www.mdpi.com/1660-3397/21/7/376 |
work_keys_str_mv | AT mengfanliao protectiveeffectandmechanismsofeckolonchroniculcerativecolitisinducedbydextransulfatesodiuminmice AT songyiwei protectiveeffectandmechanismsofeckolonchroniculcerativecolitisinducedbydextransulfatesodiuminmice AT xianminhu protectiveeffectandmechanismsofeckolonchroniculcerativecolitisinducedbydextransulfatesodiuminmice AT juanliu protectiveeffectandmechanismsofeckolonchroniculcerativecolitisinducedbydextransulfatesodiuminmice AT junwang protectiveeffectandmechanismsofeckolonchroniculcerativecolitisinducedbydextransulfatesodiuminmice |