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葛根素(Punicalagin)通过活化自噬抑制软骨细胞中叔丁基(Tert-Butyl)过氧化氢诱导的凋亡和细胞外基质降解,并减轻小鼠骨关节炎
Authors Kong J, Wang J, Gong X, Zheng X, Chen T
Received 19 September 2020
Accepted for publication 1 December 2020
Published 15 December 2020 Volume 2020:14 Pages 5521—5533
DOI https://doi.org/10.2147/DDDT.S282932
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Georgios D. Panos
Background: Osteoarthritis (OA) is a prevalent articular disorder and has no entirely satisfactory treatment. Punicalagin (PUG) is a polyphenol which has shown multiple pharmacological effects on various diseases. However, the role of PUG in the treatment of OA has not been well defined.
Methods: The effects of PUG on anti-oxidative stress, anti-apoptosis, extracellular matrix (ECM) degradation and autophagy were evaluated in chondrocytes through Western blot and immunofluorescence (IF) staining. Meanwhile, the effects of PUG on destabilization of the medial meniscus (DMM) model were also assessed in vivo by performing histopathologic analysis and IF staining.
Results: In vitro, PUG treatment not only increased the level of HO-1 and SOD1 against oxidative stress but also suppressed the expression of apoptotic proteins and inhibited ECM degradation. Meanwhile, PUG treatment activated autophagy and restores autophagic flux in chondrocytes after tert-butyl hydroperoxide (TBHP) insult, inhibition of autophagy by 3-methyladenine (3-MA) partly abrogated the protective effects of PUG on chondrocytes. In vivo, degeneration of the articular cartilage following DMM was also ameliorated by PUG treatment.
Conclusion: PUG prevents the progression of OA through inhibition of apoptosis, oxidative stress and ECM degradation in chondrocytes, which mediated by the activation of autophagy.
Keywords: punicalagin, autophagy, osteoarthritis, apoptosis, extracellular matrix