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木犀草素通过激活 AMPK-Nrf2 信号通路保护软骨细胞免受 HO 诱导的氧化损伤,从而减轻骨关节炎的进展。

Luteolin Protects Chondrocytes from HO-Induced Oxidative Injury and Attenuates Osteoarthritis Progression by Activating AMPK-Nrf2 Signaling.

机构信息

Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou 215000, China.

Department of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou 215000, China.

出版信息

Oxid Med Cell Longev. 2022 Feb 1;2022:5635797. doi: 10.1155/2022/5635797. eCollection 2022.

DOI:10.1155/2022/5635797
PMID:35154568
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8825676/
Abstract

Osteoarthritis (OA) is a chronic degenerative disease featured by cartilage erosion and inflammation. Luteolin, a member of the flavonoid family, has been shown to exert anti-inflammatory and antioxidative activities. However, the potential biological effects and underlying mechanism of luteolin on chondrocytes and OA progression remain largely elusive. In this study, the potential effect and mechanism of luteolin on OA were investigated and . Our data revealed that luteolin inhibited HO-induced cell death, apoptosis, oxidative stress, programmed necrosis, and inflammatory mediator production in primary murine chondrocytes. In addition, luteolin could activate the AMPK and Nrf2 pathways, and AMPK serves as a positive upstream regulator of Nrf2. results demonstrated the therapeutic effects of luteolin on OA in the DMM mouse model. Collectively, our findings showed that luteolin might serve as a novel and effective treatment for OA and provided a new research direction for clinical OA therapies.

摘要

骨关节炎(OA)是一种以软骨侵蚀和炎症为特征的慢性退行性疾病。木犀草素是黄酮类家族的一员,具有抗炎和抗氧化作用。然而,木犀草素对软骨细胞和 OA 进展的潜在生物学效应和作用机制在很大程度上仍不清楚。在这项研究中,研究了木犀草素对 OA 的潜在作用和机制。我们的数据显示,木犀草素抑制了 HO 诱导的原代鼠软骨细胞死亡、细胞凋亡、氧化应激、程序性坏死和炎症介质的产生。此外,木犀草素可以激活 AMPK 和 Nrf2 通路,而 AMPK 是 Nrf2 的正向上游调节因子。体内结果表明,木犀草素对 DMM 小鼠模型中的 OA 具有治疗作用。综上所述,我们的研究结果表明,木犀草素可能是一种治疗 OA 的新方法,为临床 OA 治疗提供了新的研究方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3174/8825676/6076c7f3ec01/OMCL2022-5635797.009.jpg
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