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Suppression of Th17 cell differentiation via sphingosine-1-phosphate receptor 2 by cinnamaldehyde can ameliorate ulcerative colitis

文献类型：期刊论文

作者Qu, Shu-lan1; Chen, Long1; Wen, Xue-shan1; Zuo, Jian-ping1,2; Wang, Xiao-yu1,2; Lu, Zhi-jie3,4; Yang, Yi-fu1
刊名BIOMEDICINE & PHARMACOTHERAPY
出版日期2021-02
卷号134页码:111116
关键词Cinnamaldehyde Ulcerative colitis Th17 cells S1P2 LncRNA
ISSN号0753-3322
DOI10.1016/j.biopha.2020.111116
文献子类Article
英文摘要Ulcerative colitis (UC) is chronic disease characterized by diffuse inflammation of the mucosa of the colon and rectum. Although the etiology is unknown, dysregulation of the intestinal mucosal immune system is closely related to UC. Cinnamaldehyde (CA) is a major active compound from cinnamon, is known as its antiinflammatory and antibacterial. However, little research focused on its regulatory function on immune cells in UC. Therefore, we set out to explore the modulating effects of CA on immune cells in UC. We found that CA reduced the progression of colitis through controlling the production of proinflammatory cytokines and inhibiting the proportion of Th17 cells. Furthermore, the liquid chromatography-mass spectrometry (LC-MS) method was employed for analyzing and differentiating metabolites, data showed that sphingolipid pathway has a great influence on the effect of CA on UC. Meanwhile, sphingosine-1-phosphate receptor 2 (S1P2) and Rho-GTP protein levels were downregulated in colonic tissues after CA treatment. Moreover, in vitro assays showed that CA inhibited Th17 cell differentiation and downregulated of S1P2 and Rho-GTP signaling. Notably, we found that treatment with S1P2 antagonist (JTE-013) weakened the inhibitory effect of CA on Th17 cells. Furthermore, S1P2 deficiency (S1P2-/-) blocked the effect of CA on Th17 cell differentiation. In addition, CA can also improve inflammation via lncRNA H19 and MIAT. To sum up, this study provides clear evidence that CA can ameliorate ulcerative colitis through suppressing Th17 cells via S1P2 pathway and regulating lncRNA H19 and MIAT, which further supports S1P2 as a potential drug target for immunity-mediated UC.
WOS关键词LONG NONCODING RNA ; INTESTINAL BARRIER FUNCTION ; PROTEIN-COUPLED RECEPTOR ; LYMPHOCYTE EGRESS ; EPITHELIAL-CELLS ; POTENTIAL ROLE ; HELPER-CELLS ; HIGH GLUCOSE ; ACTIVATION ; MIAT
WOS研究方向Research & Experimental Medicine ; Pharmacology & Pharmacy
语种英语
WOS记录号WOS:000612224500006
出版者ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
源URL[http://119.78.100.183/handle/2S10ELR8/309397]  
专题新药研究国家重点实验室
通讯作者Wang, Xiao-yu; Lu, Zhi-jie; Yang, Yi-fu
作者单位1.Shanghai Univ Tradit Chinese Med, Expt Ctr Sci & Technol, Shanghai 201203, Peoples R China;
2.Chinese Acad Sci, Shanghai Inst Mat Medial, Lab Antiinflammat & Immunopharmacol, State Key Lab Drug Res, Shanghai 201203, Peoples R China;
3.Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Dept Anesthesiol, Shanghai 200438, Peoples R China;
4.Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Intens Care Unit, Shanghai 200438, Peoples R China
推荐引用方式
GB/T 7714		 Qu, Shu-lan,Chen, Long,Wen, Xue-shan,et al. Suppression of Th17 cell differentiation via sphingosine-1-phosphate receptor 2 by cinnamaldehyde can ameliorate ulcerative colitis[J]. BIOMEDICINE & PHARMACOTHERAPY,2021,134:111116.
APA Qu, Shu-lan.,Chen, Long.,Wen, Xue-shan.,Zuo, Jian-ping.,Wang, Xiao-yu.,...&Yang, Yi-fu.(2021).Suppression of Th17 cell differentiation via sphingosine-1-phosphate receptor 2 by cinnamaldehyde can ameliorate ulcerative colitis.BIOMEDICINE & PHARMACOTHERAPY,134,111116.
MLA Qu, Shu-lan,et al."Suppression of Th17 cell differentiation via sphingosine-1-phosphate receptor 2 by cinnamaldehyde can ameliorate ulcerative colitis".BIOMEDICINE & PHARMACOTHERAPY 134(2021):111116.

入库方式： OAI收割

来源：上海药物研究所

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