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Nucleic Acid-Functionalized Gold Nanorods Modulate Inflammation and Dysregulated Intestinal Barriers for Treatment of Ulcerative Colitis.

作者信息

He Wanghong, Wang Yanxue, Zhao Yifan, Wu Bingqing, Chen Yilong, Jia Lu, Tan Xinfeng, Liu Yi

机构信息

Laboratory of Tissue Regeneration and Immunology and Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing 100070, China.

State Key Laboratory of Tribology in Advanced Equipment, Tsinghua University, Beijing 100084, China.

出版信息

Biomater Res. 2025 Apr 18;29:0195. doi: 10.34133/bmr.0195. eCollection 2025.

DOI:10.34133/bmr.0195
PMID:40255504
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12006742/
Abstract

Traditional oral treatments for ulcerative colitis (UC) face marked limitations including their single therapeutic effect, potential off-target interactions, and toxic side effects. In this study, we present nucleic acid-functionalized gold nanorods (NAF AuNRs), a biocompatible nanomaterial designed for the oral treatment of dextran sulfate sodium (DSS)-induced colitis. The NAF AuNRs alleviate immune responses by inhibiting pro-inflammatory macrophages and enhancing the expression of barrier proteins in intestinal epithelial cells. Due to the negatively charged nucleic acid shell, NAF AuNRs preferentially target anionic, inflamed colon tissues upon oral administration, reducing pro-inflammatory cytokine levels and promoting the recovery of intestinal barrier in DSS-induced colitis mice. Collectively, these findings suggest that NAF AuNRs represent an innovative and promising therapeutic approach for UC management, offering novel insights into the application of nucleic acid-functionalized nanomaterials.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/e789f619eead/bmr.0195.fig.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/b5081e752dfd/bmr.0195.fig.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/2b3348e3e958/bmr.0195.fig.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/48334769ec63/bmr.0195.fig.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/1c6603d8b3d4/bmr.0195.fig.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/0d4dee15c4d5/bmr.0195.fig.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/e789f619eead/bmr.0195.fig.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/b5081e752dfd/bmr.0195.fig.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/2b3348e3e958/bmr.0195.fig.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/48334769ec63/bmr.0195.fig.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/1c6603d8b3d4/bmr.0195.fig.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/0d4dee15c4d5/bmr.0195.fig.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf50/12006742/e789f619eead/bmr.0195.fig.006.jpg

相似文献

[1]
Nucleic Acid-Functionalized Gold Nanorods Modulate Inflammation and Dysregulated Intestinal Barriers for Treatment of Ulcerative Colitis.

Biomater Res. 2025-4-18

[2]
Resveratrol alleviates intestinal mucosal barrier dysfunction in dextran sulfate sodium-induced colitis mice by enhancing autophagy.

World J Gastroenterol. 2020-9-7

[3]
Tauroursodeoxycholic Acid Reverses Dextran Sulfate Sodium-Induced Colitis in Mice via Modulation of Intestinal Barrier Dysfunction and Microbiome Dysregulation.

J Pharmacol Exp Ther. 2024-6-21

[4]
Fufangxiaopi formula alleviates DSS-induced colitis in mice by inhibiting inflammatory reaction, protecting intestinal barrier and regulating intestinal microecology.

J Ethnopharmacol. 2024-1-30

[5]
Celecoxib alleviates the DSS-induced ulcerative colitis in mice by enhancing intestinal barrier function, inhibiting ferroptosis and suppressing apoptosis.

Immunopharmacol Immunotoxicol. 2024-4

[6]
Anti-inflammatory effects of Brucea javanica oil emulsion by suppressing NF-κB activation on dextran sulfate sodium-induced ulcerative colitis in mice.

J Ethnopharmacol. 2017-2-23

[7]
Protopine Alleviates Dextran Sodium Sulfate-Induced Ulcerative Colitis by Improving Intestinal Barrier Function and Regulating Intestinal Microbiota.

Molecules. 2023-7-7

[8]
Turmeric-derived nanovesicles as novel nanobiologics for targeted therapy of ulcerative colitis.

Theranostics. 2022

[9]
Effects of Orally-Administered subsp. Strain BB12 on Dextran Sodium Sulfate-Induced Colitis in Mice.

J Microbiol Biotechnol. 2018-11-28

[10]
Aloe vera mitigates dextran sulfate sodium-induced rat ulcerative colitis by potentiating colon mucus barrier.

J Ethnopharmacol. 2021-10-28

本文引用的文献

[1]
An orally administered gold nanocluster with ROS scavenging for inflammatory bowel disease treatment.

Fundam Res. 2022-7-21

[2]
Cell Membrane-Coated Nanotherapeutics for the Targeted Treatment of Acute and Chronic Colitis.

Biomater Res. 2024-11-7

[3]
Oral administration of Sophora Flavescens-derived exosomes-like nanovesicles carrying CX5461 ameliorates DSS-induced colitis in mice.

J Nanobiotechnology. 2024-10-8

[4]
Natural medicines-derived carbon dots as novel oral antioxidant administration strategy for ulcerative colitis therapy.

J Nanobiotechnology. 2024-8-27

[5]
Advanced Bioinspired Multifunctional Platforms Focusing on Gut Microbiota Regulation.

ACS Nano. 2024-8-13

[6]
Enzyme/ROS dual-sensitive nanoplatform with on-demand Celastrol release capacity for enhanced ulcerative colitis therapy by ROS scavenging, microbiota rebalancing, inflammation alleviating.

J Nanobiotechnology. 2024-7-26

[7]
Gingerenone A Attenuates Ulcerative Colitis via Targeting IL-17RA to Inhibit Inflammation and Restore Intestinal Barrier Function.

Adv Sci (Weinh). 2024-7

[8]
Red/NIR-I-Fluorescence Carbon Dots Based on Rhein with Active Oxygen Scavenging and Colitis Targeting for UC Therapeutics.

Adv Healthc Mater. 2024-7

[9]
Dual-ROS Sensitive Moieties Conjugate Inhibits Curcumin Oxidative Degradation for Colitis Precise Therapy.

Adv Healthc Mater. 2024-5

[10]
Combined biolistic and cell penetrating peptide delivery for the development of scalable intradermal DNA vaccines.

J Control Release. 2024-3

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