ArticleChinese medicine2023
Ajugol's upregulation of TFEB-mediated autophagy alleviates endoplasmic reticulum stress in chondrocytes and retards osteoarthritis progression in a mouse model.
Article in Chinese medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Programmed cell death in degenerative skeletal diseases: molecular crosstalk and combinatorial therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Rosamultin Alleviates LPS-Induced Acute Kidney Injury by Promoting Autophagy and Inhibiting the NF-κB Signaling Pathway.Drug design, development and therapy · 2026Article
- Beyond cardiovascular disease: remnant cholesterol as a novel risk factor for osteoarthritis.Frontiers in nutrition · 2025Article
- Article
- Changes in Rehmanniae Radix processing and their impact on ovarian hypofunction: potential mechanisms of action.Frontiers in pharmacology · 2024Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundOsteoarthritis (OA), a degenerative disease with a high global prevalence, is characterized by the degradation of the extracellular matrix (ECM) and the apoptosis of chondrocytes. Ajugol, a extract derived from the herb Rehmannia glutinosa, has not yet been investigated for its potential in modulating the development of OA.
methodsWe employed techniques such as western blotting, immunofluorescence, immunohistochemistry, X-ray imaging, HE staining, and SO staining to provide biological evidence supporting the role of Ajugol as a potential therapeutic agent for modulating OA. Furthermore, in an in vivo experiment, intra-peritoneal injection of 50 mg/kg Ajugol effectively mitigated the progression of OA following destabilization of the medial meniscus (DMM) surgery.
resultsOur findings revealed that treatment with 50 μM Ajugol activated TFEB-mediated autophagy, alleviating ER stress-induced chondrocyte apoptosis and ECM degradation caused by TBHP. Furthermore, in an in vivo experiment, intra-peritoneal injection of 50 mg/kg Ajugol effectively mitigated the progression of OA following destabilization of the medial meniscus (DMM) surgery.
conclusionThese results provide compelling biological evidence supporting the role of Ajugol as a potential therapeutic agent for modulating OA by activating autophagy and attenuating ER stress-induced cell death and ECM degradation. The promising in vivo results further suggest the potential of Ajugol as a treatment strategy for OA progression.
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