Ajugol's upregulation of TFEB-mediated autophagy alleviates endoplasmic reticulum stress in chondrocytes and retards osteoarthritis progression in a mouse model.
Autor: | Wu, Jingtao, Yu, Heng, Jin, Yangcan, Wang, Jingquan, Zhou, Liwen, Cheng, Teng, Zhang, Zhao, Lin, Binghao, Miao, Jiansen, Lin, Zhongke |
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Předmět: |
PHYTOTHERAPY
CARTILAGE cells DISEASE progression BIOLOGICAL models DRUG efficacy HERBAL medicine STAINS & staining (Microscopy) TERPENES IN vivo studies INJECTIONS ENDOPLASMIC reticulum AUTOPHAGY ANIMAL experimentation WESTERN immunoblotting IMMUNOHISTOCHEMISTRY GLYCOSIDES MENISCECTOMY APOPTOSIS OSTEOARTHRITIS FLUORESCENT antibody technique RESEARCH funding PLANT extracts MOLECULAR structure EXTRACELLULAR space MICE EVALUATION |
Zdroj: | Chinese Medicine; 9/7/2023, Vol. 18 Issue 1, p1-16, 16p |
Abstrakt: | Background: Osteoarthritis (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. Methods: We 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. Results: Our 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. Conclusion: These 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. [ABSTRACT FROM AUTHOR] |
Databáze: | Complementary Index |
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