Ozone induces autophagy by activating PPARγ/mTOR in rat chondrocytes treated with IL-1β

Abstract Background Osteoarthritis (OA) is the main cause of older pain and disability. Intra-articular injections of ozone (O3) commonly have been found to have antioxidative and anti-inflammatory effects to reduce pain and improve function in knee osteoarthritis. It has been reported that reduced...

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Main Authors: Panpan Sun, Weicheng Xu, Xu Zhao, Cong Zhang, Xiaowen Lin, Moxuan Gong, Zhijian Fu
Format: Article
Language:English
Published: BMC 2022-07-01
Series:Journal of Orthopaedic Surgery and Research
Subjects:
Online Access:https://doi.org/10.1186/s13018-022-03233-y
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author Panpan Sun
Weicheng Xu
Xu Zhao
Cong Zhang
Xiaowen Lin
Moxuan Gong
Zhijian Fu
author_facet Panpan Sun
Weicheng Xu
Xu Zhao
Cong Zhang
Xiaowen Lin
Moxuan Gong
Zhijian Fu
author_sort Panpan Sun
collection DOAJ
description Abstract Background Osteoarthritis (OA) is the main cause of older pain and disability. Intra-articular injections of ozone (O3) commonly have been found to have antioxidative and anti-inflammatory effects to reduce pain and improve function in knee osteoarthritis. It has been reported that reduced autophagy in chondrocytes plays an important role in the development of OA. This study aimed to probe the role of O3 on the autophagy in chondrocytes treated with IL-1β. Methods Primary chondrocytes were isolated from Wistar rats cartilage within 3 days. The OA chondrocytes model was induced via treatment with IL-1β for 24 h. Then the cells were treated with O3 and GW9662, the inhibitor of PPARγ. Cell viability was assessed by CCK-8. Further, the cells subjected to Western blot analysis, qRT-PCR and immunofluorescence assay. The numbers of autophagosomes were observed via transmission electron microscopy. Results 30 μg/ml O3 improved the viability of chondrocytes treated with IL-1β. The decreased level of autophagy proteins and the numbers of autophagosomes improved in IL-1β-treated chondrocytes with O3 via activating PPARγ/mTOR. In addition, the qRT-PCR results showed that O3 decreased the levels of IL-6, TNF-α and MMP-3, MMP-13 in chondrocytes treated with IL-1β. Conclusions 30 μg/ml O3 improved autophagy via activating PPARγ/mTOR signaling and suppressing inflammation in chondrocytes treated with IL-1β.
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spelling doaj.art-1026654161464f9ca4a3df40801e59b32022-12-22T04:23:50ZengBMCJournal of Orthopaedic Surgery and Research1749-799X2022-07-0117111110.1186/s13018-022-03233-yOzone induces autophagy by activating PPARγ/mTOR in rat chondrocytes treated with IL-1βPanpan Sun0Weicheng Xu1Xu Zhao2Cong Zhang3Xiaowen Lin4Moxuan Gong5Zhijian Fu6Department of Pain Management, The Second Hospital of Shandong UniversityDepartment of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityDepartment of Anesthesiology, Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityDepartment of Pain Management, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong UniversityDepartment of Pain Management, Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityDepartment of Anesthesiology, The Second Hospital of Shandong UniversityDepartment of Pain Management, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong UniversityAbstract Background Osteoarthritis (OA) is the main cause of older pain and disability. Intra-articular injections of ozone (O3) commonly have been found to have antioxidative and anti-inflammatory effects to reduce pain and improve function in knee osteoarthritis. It has been reported that reduced autophagy in chondrocytes plays an important role in the development of OA. This study aimed to probe the role of O3 on the autophagy in chondrocytes treated with IL-1β. Methods Primary chondrocytes were isolated from Wistar rats cartilage within 3 days. The OA chondrocytes model was induced via treatment with IL-1β for 24 h. Then the cells were treated with O3 and GW9662, the inhibitor of PPARγ. Cell viability was assessed by CCK-8. Further, the cells subjected to Western blot analysis, qRT-PCR and immunofluorescence assay. The numbers of autophagosomes were observed via transmission electron microscopy. Results 30 μg/ml O3 improved the viability of chondrocytes treated with IL-1β. The decreased level of autophagy proteins and the numbers of autophagosomes improved in IL-1β-treated chondrocytes with O3 via activating PPARγ/mTOR. In addition, the qRT-PCR results showed that O3 decreased the levels of IL-6, TNF-α and MMP-3, MMP-13 in chondrocytes treated with IL-1β. Conclusions 30 μg/ml O3 improved autophagy via activating PPARγ/mTOR signaling and suppressing inflammation in chondrocytes treated with IL-1β.https://doi.org/10.1186/s13018-022-03233-yO3OsteoarthritisPPARγ/mTORAutophagyInflammation
spellingShingle Panpan Sun
Weicheng Xu
Xu Zhao
Cong Zhang
Xiaowen Lin
Moxuan Gong
Zhijian Fu
Ozone induces autophagy by activating PPARγ/mTOR in rat chondrocytes treated with IL-1β
Journal of Orthopaedic Surgery and Research
O3
Osteoarthritis
PPARγ/mTOR
Autophagy
Inflammation
title Ozone induces autophagy by activating PPARγ/mTOR in rat chondrocytes treated with IL-1β
title_full Ozone induces autophagy by activating PPARγ/mTOR in rat chondrocytes treated with IL-1β
title_fullStr Ozone induces autophagy by activating PPARγ/mTOR in rat chondrocytes treated with IL-1β
title_full_unstemmed Ozone induces autophagy by activating PPARγ/mTOR in rat chondrocytes treated with IL-1β
title_short Ozone induces autophagy by activating PPARγ/mTOR in rat chondrocytes treated with IL-1β
title_sort ozone induces autophagy by activating pparγ mtor in rat chondrocytes treated with il 1β
topic O3
Osteoarthritis
PPARγ/mTOR
Autophagy
Inflammation
url https://doi.org/10.1186/s13018-022-03233-y
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AT congzhang ozoneinducesautophagybyactivatingppargmtorinratchondrocytestreatedwithil1b
AT xiaowenlin ozoneinducesautophagybyactivatingppargmtorinratchondrocytestreatedwithil1b
AT moxuangong ozoneinducesautophagybyactivatingppargmtorinratchondrocytestreatedwithil1b
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