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肉桂醛通过调节网蛋白-1/Deleted in Colorectal Cancer (DCC)-Unc-5同源蛋白B（UNC5B）信号转导减轻链脲佐菌素诱导的大鼠糖尿病性骨质疏松症。

Cinnamaldehyde attenuates streptozocin-induced diabetic osteoporosis in a rat model by modulating netrin-1/DCC-UNC5B signal transduction.

作者信息

Ji Songjie, Zhao Bingjia, Gao Yuan, Xie Jun, Han Huijun, Wu Qunli, Yang Dan

机构信息

Department of Orthopaedic Surgery, Beijing Jishuitan Hospital, Capital Medical University, Beijing, China.

Department of Joint Surgery, Beijing Jishuitan Guizhou Hospital, Guiyang, China.

出版信息

Front Pharmacol. 2024 Apr 2;15:1367806. doi: 10.3389/fphar.2024.1367806. eCollection 2024.

DOI:10.3389/fphar.2024.1367806
PMID:38628640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11019308/
Abstract

Cinnamaldehyde (CMD) is a major functional component of and has shown treatment effects against diverse bone diseases. This study aimed to assess the anti-diabetic osteoporosis (DOP) potential of diabetes mellitus (DM) and to explore the underlying mechanism driving the activity of CMD. A DOP model was induced via an intraperitoneal injection of streptozocin (STZ) into Sprague-Dawley rats, and then two different doses of CMD were administered to the rats. The effects of CMD on the strength, remodeling activity, and histological structure of the bones were assessed. Changes in the netrin-1 related pathways also were detected to elucidate the mechanism of the anti-DOP activity by CMD. CMD had no significant effect on the body weight or blood glucose level of the model rats. However, the data showed that CMD improved the bone strength and bone remodeling activity as well as attenuating the bone structure destruction in the DOP rats in a dose-dependent manner. The expression of netrin-1, DCC, UNC5B, RANKL, and OPG was suppressed, while the expression of TGF-β1, cathepsin K, TRAP, and RANK was induced by the STZ injection. CMD administration restored the expression of all of these indicators at both the mRNA and protein levels, indicating that the osteoclast activity was inhibited by CMD. The current study demonstrated that CMD effectively attenuated bone impairments associated with DM in a STZ-induced DOP rat model, and the anti-DOP effects of CMD were associated with the modulation of netrin-1/DCC/UNC5B signal transduction.

摘要

肉桂醛（CMD）是[某种物质]的主要功能成分，已显示出对多种骨疾病的治疗作用。本研究旨在评估肉桂醛对糖尿病（DM）所致抗糖尿病性骨质疏松症（DOP）的潜在作用，并探索其发挥作用的潜在机制。通过向Sprague-Dawley大鼠腹腔注射链脲佐菌素（STZ）诱导建立DOP模型，然后给大鼠施用两种不同剂量的CMD。评估CMD对骨骼强度、重塑活性和组织结构的影响。还检测了与netrin-1相关通路的变化，以阐明CMD抗DOP活性的机制。CMD对模型大鼠的体重或血糖水平无显著影响。然而，数据显示CMD可改善DOP大鼠的骨强度和骨重塑活性，并以剂量依赖的方式减轻骨结构破坏。STZ注射诱导netrin-1、DCC、UNC5B、RANKL和OPG的表达受到抑制，同时诱导TGF-β1、组织蛋白酶K、TRAP和RANK的表达。施用CMD可在mRNA和蛋白质水平上恢复所有这些指标的表达，表明CMD抑制了破骨细胞活性。当前研究表明，在STZ诱导的DOP大鼠模型中，CMD有效减轻了与DM相关的骨损伤，且CMD的抗DOP作用与netrin-1/DCC/UNC5B信号转导的调节有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/455c6a044de8/fphar-15-1367806-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/f667f9b1b416/fphar-15-1367806-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/4fc705037d05/fphar-15-1367806-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/2208cf6a6757/fphar-15-1367806-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/33322792acaf/fphar-15-1367806-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/de0f69be208f/fphar-15-1367806-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/455c6a044de8/fphar-15-1367806-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/f667f9b1b416/fphar-15-1367806-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/4fc705037d05/fphar-15-1367806-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/2208cf6a6757/fphar-15-1367806-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/33322792acaf/fphar-15-1367806-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/de0f69be208f/fphar-15-1367806-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28e/11019308/455c6a044de8/fphar-15-1367806-g006.jpg

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