摘要
Abstract
Objective:To investigate the impacts of honokiol(Hon)on interleukin(IL)-1β induced mitochondrial autophagy in chondrocytes by regulating PTEN induced putative kinase 1(PINK1)/Parkin signal pathway.Methods:Rat chondrocytes were cultured in vitro.After screening the optimal concentration of Hon,they were randomly divided into control group,model group,honokiol(Hon)group,cyclosporin A(CsA)group,and Hon+CsA group.Except for the control group,the other groups were treated with 10 ng/mL IL-1β to construct an in vitro osteoarthritis(OA)model.After the respective treatments,the following were measured:cell proliferation,apoptosis,ultrastructure,autophagy,relative content of reactive oxygen species(ROS),production levels of tumor necrosis factor-α(TNF-α)and IL-17,expression of autophagy and PINKl/Parkin pathway related protein of cells in each group.Results:Compared with the control group,the ultrastructure of chondrocytes in the model group was severely damaged,with the survival rate,the relative proportion of autophagosomes,the expression of microtubule-associated protein 1A/1B-light chain 3(LC3)Ⅱ/LC3Ⅰ,coiled-coil myosin-like BCL2-interacting protein(Beclin-1),PINK1,and Parkin proteins obviously lower,while the apoptosis rate,the relative content of ROS,and the levels of TNF-αand IL-17 were obviously higher.Compared with the model group,the ultrastructural damage of chondrocytes in the Hon group was reduced,with the survival rate,the relative proportion of autophagosomes,the expression of Beclin-1,PINK1,and Parkin proteins,LC3Ⅱ/LC3Ⅰ obviously higher,while the apoptosis rate,the relative content of ROS,and the levels of TNF-α and IL-17 were obviously lower.CsA treatment reversed Hon's effects,exacerbating all injury parameters.Conclusion:Hon can enhance mitophagy,suppress IL-1β-induced inflammation,reduce oxidative stress,and promote chondrocyte survival in OA through the activation of the PINK1/Parkin pathway.关键词
和厚朴酚/PTEN诱导假定激酶1/Parkin/白细胞介素-1β/关节软骨细胞/线粒体自噬Key words
honokiol/PTEN induced putative kinase 1/Parkin/interleukin-1β/articular chondrocytes/mitochondrial autophagy分类
医药卫生
