TY - JOUR
T1 - Curcumin improves regulatory T cells in gut-associated lymphoid tissue of colitis mice
AU - Zhao, Hai Mei
AU - Xu, Rong
AU - Huang, Xiao Ying
AU - Cheng, Shao Min
AU - Huang, Min Fang
AU - Yue, Hai Yang
AU - Wang, Xin
AU - Zou, Yong
AU - LYU, Aiping
AU - Liu, Duan Yong
N1 - Funding Information:
Supported by Project of National Natural Science Foundation of China, No. 81260595 and No.81460679; and Chinese Scholarship Council and Jiangxi Province as visiting scholar, No. 201408360106 and No. 201408360110; and Project of Jiangxi University of Traditional Chinese Medicine, No. JZYC15S13.
PY - 2016/6/21
Y1 - 2016/6/21
N2 - AIM: To explore the probable pathway by which curcumin (Cur) regulates the function of Treg cells by observing the expression of costimulatory molecules of dendritic cells (DCs). METHODS: Experimental colitis was induced by administering 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)/ethanol solution. Forty male C57BL/6 mice were randomly divided into four groups: normal, TNBS + Cur, TNBS + mesalazine (Mes) and TNBS groups. The mice in the TNBS + Cur and TNBS +Mes groups were treated with Cur and Mes, respectively, while those in the TNBS group were treated with physiological saline for 7 d. After treatment, the curative effect of Cur was evaluated by colonic weight, colonic length, weight index of the colon, and histological observation and score. The levels of CD4+CD25+Foxp3+ T cells (Treg cells) and costimulatory molecules of DCs were measured by flow cytometry. Also, related cytokines were analyzed by enzyme-linked immunosorbent assay. RESULTS: Cur alleviated inflammatory injury of the colonic mucosa, decreased colonic weigh and histological score, and restored colonic length. The number of Treg cells was increased, while the secretion of TNF-α, IL-2, IL-6, IL-12 p40, IL-17 and IL-21 and the expression of costimulatory molecules (CD205, CD54 [ICAM-1], TLR4, CD252[OX40 L], CD256 [RANK] and CD254 [RANK L]) of DCs were notably inhibited in colitis mice treated with Cur. CONCLUSION: Cur potentially modulates activation of DCs to enhance the suppressive functions of Treg cells and promote the recovery of damaged colonic mucosa in inflammatory bowel disease.
AB - AIM: To explore the probable pathway by which curcumin (Cur) regulates the function of Treg cells by observing the expression of costimulatory molecules of dendritic cells (DCs). METHODS: Experimental colitis was induced by administering 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)/ethanol solution. Forty male C57BL/6 mice were randomly divided into four groups: normal, TNBS + Cur, TNBS + mesalazine (Mes) and TNBS groups. The mice in the TNBS + Cur and TNBS +Mes groups were treated with Cur and Mes, respectively, while those in the TNBS group were treated with physiological saline for 7 d. After treatment, the curative effect of Cur was evaluated by colonic weight, colonic length, weight index of the colon, and histological observation and score. The levels of CD4+CD25+Foxp3+ T cells (Treg cells) and costimulatory molecules of DCs were measured by flow cytometry. Also, related cytokines were analyzed by enzyme-linked immunosorbent assay. RESULTS: Cur alleviated inflammatory injury of the colonic mucosa, decreased colonic weigh and histological score, and restored colonic length. The number of Treg cells was increased, while the secretion of TNF-α, IL-2, IL-6, IL-12 p40, IL-17 and IL-21 and the expression of costimulatory molecules (CD205, CD54 [ICAM-1], TLR4, CD252[OX40 L], CD256 [RANK] and CD254 [RANK L]) of DCs were notably inhibited in colitis mice treated with Cur. CONCLUSION: Cur potentially modulates activation of DCs to enhance the suppressive functions of Treg cells and promote the recovery of damaged colonic mucosa in inflammatory bowel disease.
KW - Costimulatory molecules
KW - Curcumin
KW - Dendritic cells
KW - Regulatory T cells
UR - http://www.scopus.com/inward/record.url?scp=84978961854&partnerID=8YFLogxK
U2 - 10.3748/wjg.v22.i23.5374
DO - 10.3748/wjg.v22.i23.5374
M3 - Journal article
C2 - 27340353
AN - SCOPUS:84978961854
SN - 1007-9327
VL - 22
SP - 5374
EP - 5383
JO - World Journal of Gastroenterology
JF - World Journal of Gastroenterology
IS - 23
ER -