Curcumin Regulated the Homeostasis of Memory T Cell and Ameliorated Dextran Sulfate Sodium-Induced Experimental Colitis.
Curcumin Regulated the Homeostasis of Memory T Cell and Ameliorated Dextran Sulfate Sodium-Induced Experimental Colitis.
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姜黄素调节记忆 T 细胞的稳态并改善硫酸葡聚糖钠诱导的实验性结肠炎。
DOI：
10.3389/fphar.2020.630244
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发表时间：
2020
影响因子：
5.6
通讯作者：
Liu DY
中科院分区：
文献类型：
--
作者：
Zhong YB;Kang ZP;Zhou BG;Wang HY;Long J;Zhou W;Zhao HM;Liu DY
免疫记忆可防止处于稳态的病原体再次入侵，而免疫记忆障碍可导致自身免疫性疾病，包括炎症性肠病。姜黄素是一种天然化合物，可有效对抗人类炎症性肠病和实验性结肠炎，但其潜在机制尚不清楚。本研究中，实验性结肠炎是由葡聚糖硫酸钠（DSS）诱导的。使用流式细胞术发现患有结肠炎的小鼠的外周血中幼稚细胞、中央记忆 T (TCM) 和效应记忆 (TEM) 细胞及其 CD4+ 和 CD8+ 亚群的百分比发生显着变化。连续给予姜黄素（100 mg/kg/天）7天后，DSS诱导的实验性结肠炎得到有效缓解，日重与初始体重比、结肠重量、病理损伤评分、促炎细胞因子IL-7、IL-15和IL-21水平、结肠粘膜溃疡和炎症浸润量均显着降低。重要的是，姜黄素显着恢复了幼稚细胞、TCM 细胞和 TEM 细胞及其 CD4+ 和 CD8+ 亚群的百分比。此外，姜黄素显着抑制JAK1/STAT5信号通路的激活，下调结肠组织中JAK1、STAT5和p-STAT5蛋白，上调PIAS1蛋白。这些结果表明姜黄素有效调节外周血中naïve细胞、TCM细胞和TEM细胞的分化，从而减轻DSS诱导的实验性结肠炎，这可能与抑制JAK1/STAT5信号活性有关。
Immune memory is protective against reinvasion by pathogens in the homeostatic state, while immune memory disorders can cause autoimmune disease, including inflammatory bowel disease. Curcumin is a natural compound shown to be effective against human inflammatory bowel disease and experimental colitis, but the underlying mechanism is unclear. Here, experimental colitis was induced by dextran sulfate sodium (DSS) in this study. Significant changes in the percentages of naïve, central memory T (TCM), and effector memory (TEM) cells and their CD4+ and CD8+ subsets were found in the peripheral blood of mice with colitis using flow cytometry. After 7 days of continuous curcumin (100 mg/kg/day) administration, the DSS-induced experimental colitis was effectively relieved, with significant decreases in the ratio of day weight to initial body weight, colonic weight, pathological injury score, levels of proinflammatory cytokines IL-7, IL-15, and IL-21, colonic mucosal ulceration, and amount of inflammatory infiltrate. Importantly, curcumin significantly restored the percentages of naïve, TCM, and TEM cells and their CD4+ and CD8+ subpopulations. In addition, curcumin significantly inhibited the activation of the JAK1/STAT5 signaling pathway, downregulation of JAK1, STAT5, and p-STAT5 proteins in colon tissue, and upregulation of PIAS1 proteins. These results suggested that curcumin effectively regulated the differentiation of naïve, TCM, and TEM cells in the peripheral blood to alleviate DSS-induced experimental colitis, which might be related to the inhibition of JAK1/STAT5 signaling activity.
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影响因子：
16.6
作者：
Belarif L;Mary C;Jacquemont L;Mai HL;Danger R;Hervouet J;Minault D;Thepenier V;Nerrière-Daguin V;Nguyen E;Pengam S;Largy E;Delobel A;Martinet B;Le Bas-Bernardet S;Brouard S;Soulillou JP;Degauque N;Blancho G;Vanhove B;Poirier N
通讯作者：
Poirier N
影响因子：
82.9
作者：
Gattinoni L;Lugli E;Ji Y;Pos Z;Paulos CM;Quigley MF;Almeida JR;Gostick E;Yu Z;Carpenito C;Wang E;Douek DC;Price DA;June CH;Marincola FM;Roederer M;Restifo NP
通讯作者：
Restifo NP
四神丸对右旋糖酐硫酸钠诱导的实验性结肠炎记忆T细胞的影响
影响因子：
5.6
作者：
Ge, Wei;Wang, Hai-Yan;Liu, Duan-Yong
通讯作者：
Liu, Duan-Yong
DOI：
10.1152/ajpgi.00496.2005
发表时间：
2006-08-01
影响因子：
4.5
作者：
Fujii, R.;Kanai, T.;Watanabe, M.
通讯作者：
Watanabe, M.
影响因子：
5.8
作者：
Gao, XH;Kuo, J;Gautam, SC
通讯作者：
Gautam, SC