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姜黄素在肠道上皮炎性损伤模型中的抗凋亡作用

Curcumin Anti-Apoptotic Action in a Model of Intestinal Epithelial Inflammatory Damage.

作者信息

Loganes Claudia, Lega Sara, Bramuzzo Matteo, Vecchi Brumatti Liza, Piscianz Elisa, Valencic Erica, Tommasini Alberto, Marcuzzi Annalisa

机构信息

Department of Paediatrics, Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Via dell'Istria 65/1, Trieste 34137, Italy.

Department of Medicine, Surgery, and Health Sciences, University of Trieste, Strada di Fiume, 447, Trieste 34100, Italy.

出版信息

Nutrients. 2017 Jun 6;9(6):578. doi: 10.3390/nu9060578.

DOI:10.3390/nu9060578
PMID:28587282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5490557/
Abstract

The purpose of this study is to determine if a preventive treatment with curcumin can protect intestinal epithelial cells from inflammatory damage induced by IFNγ. To achieve this goal we have used a human intestinal epithelial cell line (HT29) treated with IFNγ to undergo apoptotic changes that can reproduce the damage of intestinal epithelia exposed to inflammatory cytokines. In this model, we measured the effect of curcumin (curcuminoid from ) added as a pre-treatment at different time intervals before stimulation with IFNγ. Curcumin administration to HT29 culture before the inflammatory stimulus IFNγ reduced the cell apoptosis rate. This effect gradually declined with the reduction of the curcumin pre-incubation time. This anti-apoptotic action by curcumin pre-treatment was paralleled by a reduction of secreted IL7 in the HT29 culture media, while there was no relevant change in the other cytokine levels. Even though curcumin pre-administration did not impact the activation of the NF-κB pathway, a slight effect on the phosphorylation of proteins in this inflammatory signaling pathway was observed. In conclusion, curcumin pre-treatment can protect intestinal cells from inflammatory damage. These results can be the basis for studying the preventive role of curcumin in inflammatory bowel diseases.

摘要

本研究的目的是确定姜黄素的预防性治疗是否能保护肠上皮细胞免受IFNγ诱导的炎症损伤。为实现这一目标,我们使用了经IFNγ处理的人肠上皮细胞系(HT29),使其发生凋亡变化,以重现暴露于炎性细胞因子的肠上皮损伤。在该模型中,我们测量了在IFNγ刺激前不同时间间隔作为预处理添加姜黄素(来自 的姜黄素类化合物)的效果。在炎性刺激IFNγ之前向HT29培养物中施用姜黄素可降低细胞凋亡率。随着姜黄素预孵育时间的减少,这种效果逐渐下降。姜黄素预处理的这种抗凋亡作用与HT29培养基中分泌的IL7减少平行,而其他细胞因子水平没有相关变化。尽管姜黄素的预先给药不影响NF-κB途径的激活,但在该炎症信号通路中观察到对蛋白质磷酸化有轻微影响。总之,姜黄素预处理可保护肠细胞免受炎症损伤。这些结果可为研究姜黄素在炎症性肠病中的预防作用奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af9/5490557/f900c4fefa8d/nutrients-09-00578-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af9/5490557/f9d8743105e7/nutrients-09-00578-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af9/5490557/f900c4fefa8d/nutrients-09-00578-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af9/5490557/caea94feda41/nutrients-09-00578-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af9/5490557/2ac8bd0dd643/nutrients-09-00578-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af9/5490557/b277b8374aae/nutrients-09-00578-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af9/5490557/0c6957253c9c/nutrients-09-00578-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af9/5490557/85adc84ddc58/nutrients-09-00578-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af9/5490557/0286b2f149c8/nutrients-09-00578-g006.jpg
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