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EGCG 通过 TLR4/MyD88/NF-B 信号通路维持大鼠葡聚糖硫酸钠诱导的溃疡性结肠炎中的 Th1/Th2 平衡。

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

机构信息

Department of Endocrinology, General Hospital of Shenyang Military Area Command, No. 83 Wenhua Road, Shenyang, Liaoning 110016, China.

Department of Laboratory, General Hospital of Shenyang Military Area Command, No. 83 Wenhua Road, Shenyang, Liaoning 110016, China.

出版信息

Can J Gastroenterol Hepatol. 2017;2017:3057268. doi: 10.1155/2017/3057268. Epub 2017 Dec 18.

DOI:10.1155/2017/3057268
PMID:29404307
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5748319/
Abstract

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-B 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 CD4IFN- and CD4IL-4 in the spleen and colon. TLR4 antagonist E5564 was given in each group. Flow cytometry was utilized to detect CD4IFN- and CD4IL-4 cells. Immunohistochemistry, qPCR, and western blot assay were applied to measure the expression of TLR4, MyD88, and NF-B.

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-B. 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-B signaling pathway.

摘要

目的

观察表没食子儿茶素没食子酸酯（EGCG）对葡聚糖硫酸钠（DSS）诱导的大鼠溃疡性结肠炎的保护作用，并探讨 TLR4/MyD88/NF-B 信号通路的作用。

方法

通过给予 DSS 建立大鼠溃疡性结肠炎模型。给予 EGCG（50mg/kg/d）以评估疾病活动指数。HE 染色观察组织学变化。ELISA 和 qPCR 检测炎症因子的表达。流式细胞术检测脾和结肠中 CD4IFN-和 CD4IL-4 的百分比。在各组中给予 TLR4 拮抗剂 E5564。流式细胞术检测 CD4IFN-和 CD4IL-4 细胞。免疫组化、qPCR 和 Western blot 检测 TLR4、MyD88 和 NF-B 的表达。

结果

EGCG 改善了大鼠的肠黏膜损伤，抑制了炎症因子的产生，维持了 Th1/Th2 的平衡，并降低了 TLR4、MyD88 和 NF-B 的表达。TLR4 拮抗后，EGCG 对溃疡性结肠炎大鼠肠黏膜损伤的保护作用减弱，炎症因子表达上调。

结论

EGCG 可通过减轻溃疡性结肠炎的严重程度，通过 TLR4/MyD88/NF-B 信号通路维持 Th1/Th2 平衡，抑制肠道炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbec/5748319/633e88fdbbc7/CJGH2017-3057268.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbec/5748319/06777d1bba4f/CJGH2017-3057268.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbec/5748319/1452cc995706/CJGH2017-3057268.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbec/5748319/dcf62ff22fb2/CJGH2017-3057268.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbec/5748319/633e88fdbbc7/CJGH2017-3057268.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbec/5748319/06777d1bba4f/CJGH2017-3057268.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbec/5748319/1452cc995706/CJGH2017-3057268.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbec/5748319/dcf62ff22fb2/CJGH2017-3057268.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbec/5748319/633e88fdbbc7/CJGH2017-3057268.004.jpg

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