雷尼酸锶能调节环状 RNA BACH1/microRNA-155-5p,从而在牙齿矫正过程中改善牙根吸收和牙齿固定。

IF 2 4区 医学 Q3 PHYSIOLOGY
Journal of Physiology and Pharmacology Pub Date : 2024-08-01 Epub Date: 2024-10-10 DOI:10.26402/jpp.2024.4.09
N N Wang, L Li, Z Q Gu
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引用次数: 0

摘要

牙齿移动是任何正畸治疗的基本要求。本研究旨在探讨雷尼酸锶(SR)在正畸牙齿移动(OTM)中的作用和机制。研究人员每天给大鼠灌胃雷尼酸锶以及干扰 circBACH1 或 miR-155-5p 的慢病毒载体。三周后,建立了 OTM 大鼠模型。对血清中的 RANKL 和骨保护素(OpG)进行了测定。检查第一和第二磨牙之间的间隙以及牙根吸收情况。使用破骨细胞测试;并检查牙根状况。检测了 miR-155-5p、circBACH1、CLC7 和 cathepsin K。验证了 circBACH1 与 miR-155-5p 的结合。在 OTM 大鼠中,circBACH1 升高(p
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Strontium ranelate modulates circular RNA BACH1/microRNA-155-5p to ameliorate root resorption and tooth anchoring during orthodontic tooth movement.

The tooth movement is a fundamental requirement during any orthodontic treatment. This study aimed to investigate the action and mechanism of strontium ranelate (SR) in orthodontic tooth movement (OTM). Rats were given SR by gavage daily, along with lentiviral vectors interfering with circBACH1 or miR-155-5p. Three weeks later, an OTM rat model was established. RANKL and osteoprotegerin (OpG) in serum were measured. The gap between the first and second molar and root resorption were examined. Osteoclast test was used; and root condition was examined. Detection of miR-155-5p, circBACH1, CLC7 and cathepsin K was performed. The binding of circBACH1 to miR-155-5p was verified. In OTM rats, circBACH1 was elevated (p<0.05) and miR-155-5p was silenced (p<0.05). SR reduced osteoclast activity (p<0.05) and improved root resorption (p<0.05) in OTM rats, which was enhanced by silenced circBACH1 (p<0.05) or elevated miR-155-5p (p<0.05). circBACH1 inhibited miR-155-5p expression (p<0.05). Silenced miR-155-5p reversed the ameliorative effect of circBACH1 on tooth root resorption in OTM rats (all p<0.05). SR modulates circBACH1/miR-155-5p to ameliorate root resorption and tooth fixation during OTM.

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来源期刊
CiteScore
4.00
自引率
22.70%
发文量
0
审稿时长
6-12 weeks
期刊介绍: Journal of Physiology and Pharmacology publishes papers which fall within the range of basic and applied physiology, pathophysiology and pharmacology. The papers should illustrate new physiological or pharmacological mechanisms at the level of the cell membrane, single cells, tissues or organs. Clinical studies, that are of fundamental importance and have a direct bearing on the pathophysiology will also be considered. Letters related to articles published in The Journal with topics of general professional interest are welcome.
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