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...
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Wiley
2017-01-01
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Series: | Canadian Journal of Gastroenterology and Hepatology |
Online Access: | http://dx.doi.org/10.1155/2017/3057268 |
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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. |
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institution | Kabale University |
issn | 2291-2789 2291-2797 |
language | English |
publishDate | 2017-01-01 |
publisher | Wiley |
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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 |
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