Astragalin mitigates inflammatory osteolysis by negatively modulating osteoclastogenesis via ROS and MAPK signaling pathway

Xing, Fangze; Geng, Luying; Guan, Huanshuai; Liu, Donghua; Li, Yiyang; Zeng, Lizhong; Chen, Yang; Tian, Run; Li, Zhe; Cao, Ruomu; Zhao, Yiwei; Yan, Ping; Qiang, Hui; Kong, Ning; Wang, Kunzheng; Yang, Pei

doi:10.1016/j.intimp.2022.109278

Cited by 17 publications

(9 citation statements)

References 36 publications

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“…Recent study has implied that tricalcium phosphate particles promote calvarial osteocyte pyroptosis through the ROS/NLRP3/caspase‐1 pathway to promote osteoclastogenesis (Zhang et al, 2022). In addition, astragalin negatively regulates osteoclastogenesis by inhibiting the ROS signaling pathway, thereby attenuating LPS‐induced bone loss in a mouse model (Xing et al, 2022). As a multifunctional protein, apelin‐13 not only attenuates acute lung injury by regulating NOX4‐dependent ROS (Yuan et al, 2022), but also exerts neuroprotective effects by antioxidative stress (Chen et al, 2023).…”

Section: Discussionmentioning

confidence: 99%

Apelin‐13 alleviates osteoclast formation and osteolysis through Nrf2‐pyroptosis pathway

Yin,

Cheng,

Wang

et al. 2024

Microscopy Res & Technique

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Wear particle‐induced periprosthetic osteolysis is the key to aseptic loosening after artificial joint replacement. Osteoclastogenesis plays a central role in this process. Apelin‐13 is a member of the adipokine family with anti‐inflammatory effects. Here, we report that apelin‐13 alleviates RANKL‐mediated osteoclast differentiation and titanium particle‐induced osteolysis in mouse calvaria. Mechanistically, apelin‐13 inhibits NLRP3 inflammasome‐mediated pyroptosis by activating the nuclear factor erythroid 2‐related factor 2 (Nrf2) pathway. In summary, apelin‐13 is expected to be a potential drug for relieving aseptic osteolysis.Research Highlights This study reveals the molecular mechanism by which apelin‐13 inhibits NLRP3 inflammasome activation and pyroptosis by promoting Nrf2. This study confirms that apelin‐13 alleviates osteoclast activation by inhibiting pyroptosis. In vivo studies further confirmed that apelin‐13 alleviated mouse skull osteolysis by inhibiting the activation of NLRP3 inflammasome.

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Section: Discussionmentioning

confidence: 99%

Apelin‐13 alleviates osteoclast formation and osteolysis through Nrf2‐pyroptosis pathway

Yin,

Cheng,

Wang

et al. 2024

Microscopy Res & Technique

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“…Meanwhile, its anti‐inflammation bioactivity through inhibiting MAPK has also been reported in different models (Jia et al, 2019; Ma et al, 2015). Furthermore, Xing et al (2022) reported that astragalin inhibits RANKL‐ and lipopolysaccharides (LPS)‐induced osteoclastogenesis in vitro by downregulating MAPK and ROS signaling pathways during osteoclast differentiation thereby suppressing inflammatory osteolysis.…”

Section: Methodsmentioning

confidence: 99%

Natural anti‐inflammatory products for osteoarthritis: From molecular mechanism to drug delivery systems and clinical trials

Su,

Yu,

Wang

et al. 2023

Phytotherapy Research

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Osteoarthritis (OA) is a degenerative joint disease that affects millions globally. The present nonsteroidal anti‐inflammatory drug treatments have different side effects, leading researchers to focus on natural anti‐inflammatory products (NAIPs). To review the effectiveness and mechanisms of NAIPs in the cellular microenvironment, examining their impact on OA cell phenotype and organelles levels. Additionally, we summarize relevant research on drug delivery systems and clinical randomized controlled trials (RCTs), to promote clinical studies and explore natural product delivery options. English‐language articles were searched on PubMed using the search terms “natural products,” “OA,” and so forth. We categorized search results based on PubChem and excluded “natural products” which are mix of ingredients or compounds without the structure message. Then further review was separately conducted for molecular mechanisms, drug delivery systems, and RCTs later. At present, it cannot be considered that NAIPs can thoroughly prevent or cure OA. Further high‐quality studies on the anti‐inflammatory mechanism and drug delivery systems of NAIPs are needed, to determine the appropriate drug types and regimens for clinical application, and to explore the combined effects of different NAIPs to prevent and treat OA.

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“…Jiang et al demonstrated that PD0325901, a specific inhibitor of ERK, inhibited the expression of c-Fos and NFATc1, and suppressed osteoclast differentiation in a time-dependent and dose-dependent manner (Jiang et al 2023 ). Xing et al found that astragalin (AST), a bioactive component of Rosa agrestis, negatively regulated the MAPK signaling pathway and inhibited the expression of c-Fos and NFATc1 at different stages, resulting in reduced bone destruction in mice (Xing et al 2022 ). Moreover, Jia et al found that AST could inhibit the expression of proteins related to bone destruction such as MMP-1, MMP-3, and MMP-13 in fibroblast-like synoviocytes derived from RA patients (MH7A cells) (Jia et al 2019 ).…”

Section: The Rankl/rank Signaling Pathway Activates Nfatc1mentioning

confidence: 99%

Recent advances of NFATc1 in rheumatoid arthritis-related bone destruction: mechanisms and potential therapeutic targets

Zheng,

Liu,

Deng

et al. 2024

Mol Med

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Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease characterized by inflammation of the synovial tissue and joint bone destruction, often leading to significant disability. The main pathological manifestation of joint deformity in RA patients is bone destruction, which occurs due to the differentiation and proliferation of osteoclasts. The transcription factor nuclear factor-activated T cell 1 (NFATc1) plays a crucial role in this process. The regulation of NFATc1 in osteoclast differentiation is influenced by three main factors. Firstly, NFATc1 is activated through the upstream nuclear factor kappa-B ligand (RANKL)/RANK signaling pathway. Secondly, the Ca2+-related co-stimulatory signaling pathway amplifies NFATc1 activity. Finally, negative regulation of NFATc1 occurs through the action of cytokines such as B-cell Lymphoma 6 (Bcl-6), interferon regulatory factor 8 (IRF8), MAF basic leucine zipper transcription factor B (MafB), and LIM homeobox 2 (Lhx2). These three phases collectively govern NFATc1 transcription and subsequently affect the expression of downstream target genes including TRAF6 and NF-κB. Ultimately, this intricate regulatory network mediates osteoclast differentiation, fusion, and the degradation of both organic and inorganic components of the bone matrix. This review provides a comprehensive summary of recent advances in understanding the mechanism of NFATc1 in the context of RA-related bone destruction and discusses potential therapeutic agents that target NFATc1, with the aim of offering valuable insights for future research in the field of RA. To assess their potential as therapeutic agents for RA, we conducted a drug-like analysis of potential drugs with precise structures.

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Astragalin mitigates inflammatory osteolysis by negatively modulating osteoclastogenesis via ROS and MAPK signaling pathway

Cited by 17 publications

References 36 publications

Apelin‐13 alleviates osteoclast formation and osteolysis through Nrf2‐pyroptosis pathway

Apelin‐13 alleviates osteoclast formation and osteolysis through Nrf2‐pyroptosis pathway

Natural anti‐inflammatory products for osteoarthritis: From molecular mechanism to drug delivery systems and clinical trials

Recent advances of NFATc1 in rheumatoid arthritis-related bone destruction: mechanisms and potential therapeutic targets

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