吲哚乙酰化高直链玉米淀粉改善溃疡性结肠炎的作用机制研究

doi:10.3976/j.issn.1002-4026.20230176

Abstract

Abstract:

The aim of this study is to investigate the mechanism action of indole acetylated high-amylose maize starch in improving ulcerative colitis. Dextran sulfate sodium salt was used to induce acute ulcerative colitis in mice. Indole acetylated high-amylose maize starch was then used to target the colon with the delivery of indole-3-acetic acid. This was combined with the administration of an aryl hydrocarbon receptor inhibitor to analyze the mice in terms of colon length; disease activity index; and levels of interleukin-6, interleukin-10, transforming growth factor β1, myeloperoxidase, and interleukin-22 in the colon, which were detected by enzyme-linked immunosorbent assay. Quantitative polymerase chain reaction was used to analyze the relative expression levels of the colonic tight junction proteins occludin, ZO-1, and CYP1A1. Flow cytometry was used to test the ratio of regulatory T cells and T helper 17 cells in the mesenteric lymph nodes. The results showed that administration of indole acetylated high-amylose maize starch significantly alleviated the shortening of the colon length; significantly reduced the disease activity index and the levels of interleukin-6 and myeloperoxidase; significantly promoted the expression of interleukin-10, transforming growth factor β1, interleukin-22, CYP1A1, occludin, and ZO-1; significantly increased the proportion of regulatory T cells; and significantly reduced the proportion of T helper 17 cells. Administration of the aryl hydrocarbon receptor inhibitor weakened the effect of indole acetylated high-amylose maize starch. These results together suggest that acetylated high-amylose maize starch can improve ulcerative colitis by activating aryl hydrocarbon receptors.

Key words: microbiota metabolites, indole-3-acetic acid, ulcerative colitis, aryl hydrocarbon receptors, inflammatory response, immune balance, tryptophan

CLC Number:

R967

QU Xinyan, LI Qingjun, DING Xingchun, SONG Yingying. Mechanism of action indole acetylated high-amylose maize starch in improving ulcerative colitis[J].Shandong Science, 2024, 37(5): 17-24.

Figures/Tables 8

Table 1

Table 2

Fig.1

Fig.2

Fig.3

Fig.4

Fig.5

Fig.6

References 21

[1]	NG S C, SHI H Y, HAMIDI N, et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies[J]. The Lancet, 2017, 390(10114): 2769-2778. DOI: 10.1016/S0140-6736(17)32448-0.
[2]	KAPLAN G G. Colon cancer in Asian patients with ulcerative colitis[J]. The Lancet Gastroenterology & Hepatology, 2017, 2(4): 238-239. DOI: 10.1016/S2468-1253(17)30032-8.
[3]	OLÉN O, ERICHSEN R, SACHS M C, et al. Colorectal cancer in ulcerative colitis: a Scandinavian population-based cohort study[J]. Lancet, 2020, 395(10218): 123-131. DOI: 10.1016/S0140-6736(19)32545-0. pmid: 31929014
[4]	LAHARIE D. Towards therapeutic choices in ulcerative colitis[J]. Lancet, 2017, 390(10090): 98-99. DOI: 10.1016/S0140-6736(17)31263-1. pmid: 28527707
[5]	DANESE S, FIOCCHI C. Ulcerative colitis[J]. New England Journal of Medicine, 2011, 365(18): 1713-1725. DOI: 10.1056/nejmra1102942.
[6]	MOURÃO L R M B, SANTANA R S S, PAULO L M, et al. Protective action of indole-3-acetic acid on induced hepatocarcinoma in mice[J]. Cell Biochemistry and Function, 2009, 27(1): 16-22. DOI: 10.1002/cbf.1528. pmid: 19107877
[7]	TINTELNOT J, XU Y, LESKER T R, et al. Microbiota-derived 3-IAA influences chemotherapy efficacy in pancreatic cancer[J]. Nature, 2023, 615(7950): 168-174. DOI: 10.1038/s41586-023-05728-y.
[8]	HENDRIKX T, DUAN Y, WANG Y H, et al. Bacteria engineered to produce IL-22 in intestine induce expression of REG3G to reduce ethanol-induced liver disease in mice[J]. Gut, 2019, 68(8): 1504-1515. DOI: 10.1136/gutjnl-2018-317232. pmid: 30448775
[9]	YANG C C, DU Y, REN D Y, et al. Gut microbiota-dependent catabolites of tryptophan play a predominant role in the protective effects of turmeric polysaccharides against DSS-induced ulcerative colitis[J]. Food & Function, 2021, 12(20): 9793-9807. DOI: 10.1039/d1fo01468d.
[10]	WANG Y, JI X G, ZHAO M Y, et al. Modulation of tryptophan metabolism via AHR-IL22 pathway mediates the alleviation of DSS-induced colitis by chitooligosaccharides with different degrees of polymerization[J]. Carbohydrate Polymers, 2023, 319: 121180. DOI: 10.1016/j.carbpol.2023.121180.
[11]	YANG W Q, REN D Y, SHAO H J, et al. Theabrownin from fu brick tea improves ulcerative colitis by shaping the gut microbiota and modulating the tryptophan metabolism[J]. Journal of Agricultural and Food Chemistry, 2023, 71(6): 2898-2913. DOI: 10.1021/acs.jafc.2c06821. pmid: 36728562
[12]	ZHANG X N, SHI L, WANG N, et al. Gut bacterial indole-3-acetic acid induced immune promotion mediates preventive effects of fu brick tea polyphenols on experimental colitis[J]. Journal of Agricultural and Food Chemistry, 2023, 71(2): 1201-1213. DOI: 10.1021/acs.jafc.2c06517. pmid: 36621895
[13]	ESSER C, RANNUG A. The aryl hydrocarbon receptor in barrier organ physiology, immunology, and toxicology[J]. Pharmacological Reviews, 2015, 67(2): 259-279. DOI: 10.1124/pr.114.009001. pmid: 25657351
[14]	GUTIÉRREZ-VÁZQUEZ C, QUINTANA F J. Regulation of the immune response by the aryl hydrocarbon receptor[J]. Immunity, 2018, 48(1): 19-33. DOI: 10.1016/j.immuni.2017.12.012.
[15]	CAI J, SUN L L, GONZALEZ F J. Gut microbiota-derived bile acids in intestinal immunity, inflammation, and tumorigenesis[J]. Cell Host & Microbe, 2022, 30(3): 289-300. DOI: 10.1016/j.chom.2022.02.004.
[16]	黄志斌. 肠道菌群代谢产物吲哚丙酸部分激活芳香烃受体促进巨噬细胞吞噬减轻脓毒症损伤[D]. 广州: 南方医科大学, 2022.
[17]	姜旭, 杨华夏, 张奉春. 肠道菌群代谢产物在自身免疫性疾病中的作用[J]. 协和医学杂志, 2022, 13(5): 747-752. DOI: 10.12290/xhyxzz.2022-0246.
[18]	穆燕菊, 罗娟, 缪应雷. 基于肠道菌群参与的炎症性肠病色氨酸代谢的研究进展[J]. 国际消化病杂志, 2022, 42(3): 141-145. DOI: 10.3969/j.issn.1673-534X.2022.03.001.
[19]	SLIFER Z M, BLIKSLAGER A T. The integral role of tight junction proteins in the repair of injured intestinal epithelium[J]. International Journal of Molecular Sciences, 2020, 21(3): 972. DOI: 10.3390/ijms21030972.
[20]	BERTIN S, AOKI-NONAKA Y, LEE J, et al. The TRPA1 ion channel is expressed in CD4⁺ T cells and restrains T-cell-mediated colitis through inhibition of TRPV1[J]. Gut, 2017, 66(9): 1584-1596. DOI: 10.1136/gutjnl-2015-310710.
[21]	BRITTON G J, CONTIJOCH E J, MOGNO I, et al. Microbiotas from humans with inflammatory bowel disease alter the balance of gut Th17 and RORγt⁺ regulatory T cells and exacerbate colitis in mice[J]. Immunity, 2019, 50(1): 212-224.e4. DOI: 10.1016/j.immuni.2018.12.015.

Metrics

Comments

Recommended 0

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0), which permits third parties to freely share (i.e., copy and redistribute the material in any medium or format) and adapt (i.e., remix, transform, or build upon the material) the articles published in this journal, provided that appropriate credit is given, a link to the license is provided, and any changes made are indicated. The material may not be used for commercial purposes. For details of the CC BY-NC 4.0 license, please visit: https://creativecommons.org/licenses/by-nc/4.0

得分	体重下降/%	大便性状	粪便出血
0	≤1	正常	阴性
1	>1~5	松散	隐血阳性
2	>5~10	松散	隐血阳性
3	>10~20	稀便	肉眼血便
4	>20	稀便	肉眼血便

CD4⁺T细胞亚群	细胞表型特征
Naïve CD4⁺ T	CD3⁺ B220^- CD4⁺ CD8^- CD25^- CD44^low CD62L^high
Treg	CD3⁺ B220^- CD4⁺ CD8^- CD25⁺ FoxP3⁺
Th17	CD3⁺ B220^- CD4⁺ CD8^- CD25^- CD44⁺ IL-17a⁺

Mechanism of action indole acetylated high-amylose maize starch in improving ulcerative colitis

RichHTML

PDF (PC)

Like

Knowledge

Abstract

Cite this article

share this article

Figures/Tables 8

References 21

Related Articles 3

Metrics

Comments

Recommended 0

[1]	LUO Yaqin, HUANG Wei. Progress in the research on the mechanism of action of Scutellaria baicalensis and its active ingredients in treating ulcerative colitis [J]. Shandong Science, 2024, 37(2): 20-28.
[2]	MU Nana, LIAO Binbin, LI Zhen, LI Jipin, LI Yihua, WANG Ying, CHEN Xubing. Investigating the mechanism of action of Elephantopus scaber L. in the treatment of ulcerative colitis based on network pharmacology and molecular docking [J]. Shandong Science, 2023, 36(6): 48-55.
[3]	LIANG Jiahao, ZHANG Xinhui, WANG Hai. Exploringtrait genes and predicting the targeted Chinese medicine for ulcerative colitis based on bioinformatics and machine learning [J]. Shandong Science, 2023, 36(6): 56-67.