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基于四面体型核酸框架的 microRNA-155 递送来通过靶向 Bcl-2/Bax 凋亡途径缓解椎间盘退变。

Tetrahedral framework nucleic acids-based delivery of microRNA-155 alleviates intervertebral disc degeneration through targeting Bcl-2/Bax apoptosis pathway.

机构信息

Department of Orthopedic Surgery and Orthopedic Research Institute, West China Hospital, Sichuan University, Chengdu, China.

Department of Spine Surgery, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.

出版信息

Cell Prolif. 2024 Nov;57(11):e13689. doi: 10.1111/cpr.13689. Epub 2024 Jun 20.

DOI:10.1111/cpr.13689
PMID:38899529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11533059/
Abstract

Intervertebral disc degeneration (IDD) is one of the most common causes of chronic low back pain, which does great harm to patients' life quality. At present, the existing treatment options are mostly aimed at relieving symptoms, but the long-term efficacy is not ideal. Tetrahedral framework nucleic acids (tFNAs) are regarded as a type of nanomaterial with excellent biosafety and prominent performance in anti-apoptosis and anti-inflammation. MicroRNA155 is a non-coding RNA involved in various biological processes such as cell proliferation and apoptosis. In this study, a complex named TR155 was designed and synthesised with microRNA155 attached to the vertex of tFNAs, and its effects on the nucleus pulposus cells of intervertebral discs were evaluated both in vitro and in vivo. The experimental results showed that TR155 was able to alleviate the degeneration of intervertebral disc tissue and inhibit nucleus pulposus cell apoptosis via Bcl-2/Bax pathway, indicating its potential to be a promising option for the treatment of IDD.

摘要

椎间盘退变(IDD)是慢性腰痛的最常见原因之一,对患者的生活质量造成了极大的危害。目前,现有的治疗方法大多旨在缓解症状,但长期疗效并不理想。四面体框架核酸(tFNAs)被认为是一种具有优异生物安全性和在抗细胞凋亡和抗炎方面突出性能的纳米材料。microRNA155 是一种参与细胞增殖和凋亡等多种生物学过程的非编码 RNA。在这项研究中,设计并合成了一种名为 TR155 的复合物,将 microRNA155 连接到 tFNAs 的顶点上,并在体外和体内评估了其对椎间盘髓核细胞的影响。实验结果表明,TR155 能够通过 Bcl-2/Bax 通路减轻椎间盘组织退变和抑制髓核细胞凋亡,表明其具有治疗 IDD 的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844f/11533059/7553d10a0c38/CPR-57-e13689-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844f/11533059/12ae3d5a0b02/CPR-57-e13689-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844f/11533059/7553d10a0c38/CPR-57-e13689-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844f/11533059/12ae3d5a0b02/CPR-57-e13689-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844f/11533059/c5a2a3108ea3/CPR-57-e13689-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844f/11533059/2e6714cb100d/CPR-57-e13689-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844f/11533059/b217237fbaaa/CPR-57-e13689-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844f/11533059/7553d10a0c38/CPR-57-e13689-g006.jpg

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本文引用的文献

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