EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in Rats

Objective. To observe the protective effect of epigallocatechin gallate (EGCG) on dextran sulfate sodium- (DSS-) induced ulcerative colitis in rats and to explore the roles of TLR4/MyD88/NF-κB signaling pathway. Methods. Rat models of ulcerative colitis were established by giving DSS. EGCG (50 mg/kg...

Full description

Saved in:
Bibliographic Details
Main Authors: Xue Bing, Liu Xuelei, Dong Wanwei, Liang Linlang, Chen Keyan
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Canadian Journal of Gastroenterology and Hepatology
Online Access:http://dx.doi.org/10.1155/2017/3057268
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832546506449616896
author Xue Bing
Liu Xuelei
Dong Wanwei
Liang Linlang
Chen Keyan
author_facet Xue Bing
Liu Xuelei
Dong Wanwei
Liang Linlang
Chen Keyan
author_sort Xue Bing
collection DOAJ
description Objective. To observe the protective effect of epigallocatechin gallate (EGCG) on dextran sulfate sodium- (DSS-) induced ulcerative colitis in rats and to explore the roles of TLR4/MyD88/NF-κB signaling pathway. Methods. Rat models of ulcerative colitis were established by giving DSS. EGCG (50 mg/kg/d) was given to assess disease activity index. HE staining was applied to observe histological changes. ELISA and qPCR detected the expression of inflammatory factors. Flow cytometry was used to measure the percentage of CD4+IFN-γ+ and CD4+IL-4+ in the spleen and colon. TLR4 antagonist E5564 was given in each group. Flow cytometry was utilized to detect CD4+IFN-γ+ and CD4+IL-4+ cells. Immunohistochemistry, qPCR, and western blot assay were applied to measure the expression of TLR4, MyD88, and NF-κB. Results. EGCG improved the intestinal mucosal injury in rats, inhibited production of inflammatory factors, maintained the balance of Th1/Th2, and reduced the expression of TLR4, MyD88, and NF-κB. After TLR4 antagonism, the protective effect of EGCG on intestinal mucosal injury was weakened in rats with ulcerative colitis, and the expressions of inflammatory factors were upregulated. Conclusion. EGCG can inhibit the intestinal inflammatory response by reducing the severity of ulcerative colitis and maintaining the Th1/Th2 balance through the TLR4/MyD88/NF-κB signaling pathway.
format Article
id doaj-art-0d0643bd344d4978a332da58c9ad2229
institution Kabale University
issn 2291-2789
2291-2797
language English
publishDate 2017-01-01
publisher Wiley
record_format Article
series Canadian Journal of Gastroenterology and Hepatology
spelling doaj-art-0d0643bd344d4978a332da58c9ad22292025-02-03T06:48:06ZengWileyCanadian Journal of Gastroenterology and Hepatology2291-27892291-27972017-01-01201710.1155/2017/30572683057268EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in RatsXue Bing0Liu Xuelei1Dong Wanwei2Liang Linlang3Chen Keyan4Department of Endocrinology, General Hospital of Shenyang Military Area Command, No. 83 Wenhua Road, Shenyang, Liaoning 110016, ChinaDepartment of Laboratory, General Hospital of Shenyang Military Area Command, No. 83 Wenhua Road, Shenyang, Liaoning 110016, ChinaDepartment of Laboratory Animal Science, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, ChinaDepartment of Endocrinology, General Hospital of Shenyang Military Area Command, No. 83 Wenhua Road, Shenyang, Liaoning 110016, ChinaDepartment of Laboratory Animal Science, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, ChinaObjective. To observe the protective effect of epigallocatechin gallate (EGCG) on dextran sulfate sodium- (DSS-) induced ulcerative colitis in rats and to explore the roles of TLR4/MyD88/NF-κB signaling pathway. Methods. Rat models of ulcerative colitis were established by giving DSS. EGCG (50 mg/kg/d) was given to assess disease activity index. HE staining was applied to observe histological changes. ELISA and qPCR detected the expression of inflammatory factors. Flow cytometry was used to measure the percentage of CD4+IFN-γ+ and CD4+IL-4+ in the spleen and colon. TLR4 antagonist E5564 was given in each group. Flow cytometry was utilized to detect CD4+IFN-γ+ and CD4+IL-4+ cells. Immunohistochemistry, qPCR, and western blot assay were applied to measure the expression of TLR4, MyD88, and NF-κB. Results. EGCG improved the intestinal mucosal injury in rats, inhibited production of inflammatory factors, maintained the balance of Th1/Th2, and reduced the expression of TLR4, MyD88, and NF-κB. After TLR4 antagonism, the protective effect of EGCG on intestinal mucosal injury was weakened in rats with ulcerative colitis, and the expressions of inflammatory factors were upregulated. Conclusion. EGCG can inhibit the intestinal inflammatory response by reducing the severity of ulcerative colitis and maintaining the Th1/Th2 balance through the TLR4/MyD88/NF-κB signaling pathway.http://dx.doi.org/10.1155/2017/3057268
spellingShingle Xue Bing
Liu Xuelei
Dong Wanwei
Liang Linlang
Chen Keyan
EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in Rats
Canadian Journal of Gastroenterology and Hepatology
title EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in Rats
title_full EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in Rats
title_fullStr EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in Rats
title_full_unstemmed EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in Rats
title_short EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in Rats
title_sort egcg maintains th1 th2 balance and mitigates ulcerative colitis induced by dextran sulfate sodium through tlr4 myd88 nf κb signaling pathway in rats
url http://dx.doi.org/10.1155/2017/3057268
work_keys_str_mv AT xuebing egcgmaintainsth1th2balanceandmitigatesulcerativecolitisinducedbydextransulfatesodiumthroughtlr4myd88nfkbsignalingpathwayinrats
AT liuxuelei egcgmaintainsth1th2balanceandmitigatesulcerativecolitisinducedbydextransulfatesodiumthroughtlr4myd88nfkbsignalingpathwayinrats
AT dongwanwei egcgmaintainsth1th2balanceandmitigatesulcerativecolitisinducedbydextransulfatesodiumthroughtlr4myd88nfkbsignalingpathwayinrats
AT lianglinlang egcgmaintainsth1th2balanceandmitigatesulcerativecolitisinducedbydextransulfatesodiumthroughtlr4myd88nfkbsignalingpathwayinrats
AT chenkeyan egcgmaintainsth1th2balanceandmitigatesulcerativecolitisinducedbydextransulfatesodiumthroughtlr4myd88nfkbsignalingpathwayinrats