分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

Punicalagin Inhibits Tert-Butyl Hydroperoxide-Induced Apoptosis and Extracellular Matrix Degradation in Chondrocytes by Activating Autophagy and Ameliorates Murine Osteoarthritis

Jinsong Kong, Jiacheng Wang, Xiaokang Gong, Xin Zheng, Tao Chen

Journal:Drug Design Development and Therapy

IF:4.32

DOI:10.2147/DDDT.S282932

PMID:33364748

Published:2022-10-31

research field:细胞生物学遗传学与基因组学生物化学

Abstract

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.

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