Han Qingxin, Wu Junying, Li Yan, Tong Yi, Liu Xiaohua, Hu Xiaoqing, Zhang Lei
Department of Sports Medicine, Wangjing Hospital of China Academy of Chinese Medical Sciences, Beijing, China.
Department of Sports Medicine, Peking University Third Hospital, Beijing, China.
Front Pharmacol. 2025 Jul 8;16:1623455. doi: 10.3389/fphar.2025.1623455. eCollection 2025.
The purpose of this study is to demonstrate the effectiveness of Notoginsenoside R1 (NGR1) in treating tendinopathy and to reveal its potential mechanisms.
This study performed a preliminary network-based assessment of the potential targets that NGR1-associated in the treatment of tendinopathy, which includes PPI network analysis, GO enrichment, KEGG pathway enrichment analysis, and molecular docking. The therapeutic efficacy of NGR1 was then assessed using a collagenase-induced rat model of tendinopathy. Furthermore, the underlying mechanism was explored through LPS-induced inflammatory responses in tenocytes
Network-based assessment indicated that key targets associated with NGR1 in treating tendinopathy may potentially include IL-6, TNF, and MMP9. studies revealed that NGR1 mitigates the pathological response of tendinopathy induced by collagenase, exhibiting a dose-dependent efficacy, with the 8 μM concentration yielding the most favorable outcomes. RNA sequencing analyses of tenocytes indicated that NGR1 potentially treats tendinopathy by modulating the synthesis of collagen and matrix metalloproteinases, as well as attenuating LPS-induced inflammatory responses. These findings aligned with results obtained from quantitative PCR, ELISA and Western blot analyses.
NGR1 effectively moderates the progression of tendinopathy by modulating inflammatory reactions and matrix metabolism. This discovery offers a promising approach for clinical management of tendinopathy.
本研究旨在证明三七皂苷R1（NGR1）治疗肌腱病的有效性，并揭示其潜在机制。
本研究对NGR1治疗肌腱病相关的潜在靶点进行了基于网络的初步评估，包括蛋白质-蛋白质相互作用（PPI）网络分析、基因本体（GO）富集分析、京都基因与基因组百科全书（KEGG）通路富集分析和分子对接。然后使用胶原酶诱导的大鼠肌腱病模型评估NGR1的治疗效果。此外，通过脂多糖（LPS）诱导的肌腱细胞炎症反应探索其潜在机制。
基于网络的评估表明，NGR1治疗肌腱病相关的关键靶点可能包括白细胞介素-6（IL-6）、肿瘤坏死因子（TNF）和基质金属蛋白酶9（MMP9）。研究表明，NGR1减轻了胶原酶诱导的肌腱病病理反应，呈现剂量依赖性疗效，8 μM浓度产生最有利的结果。肌腱细胞的RNA测序分析表明，NGR1可能通过调节胶原蛋白和基质金属蛋白酶的合成以及减轻LPS诱导的炎症反应来治疗肌腱病。这些发现与定量PCR、酶联免疫吸附测定（ELISA）和蛋白质印迹分析结果一致。
NGR1通过调节炎症反应和基质代谢有效缓解肌腱病的进展。这一发现为肌腱病的临床管理提供了一种有前景的方法。
