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Research article
Ozone Induces Autophagy by Activating PPARγ/mTOR in Rat Chondrocytes Treated with IL-1β
Zhijian Fu
Shandong Provincial Hospital
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Osteoarthritis (OA) is the main cause of older pain and disability, its dysfunction due to discomfort as well as the quality of life of patients having adverse effects. Medical ozone (O3) has been found to have antioxidative and anti-inflammatory effects in the treatment of osteoarthritis. However, it is unclear whether O3 can induces autophagy through the PPARγ/mTOR autophagy pathway in chondrocytes treated with IL-1β.
Methods: Primary chondrocytes were isolated from wistar rat cartilage within 3days. The OA chondrocyte model was induced via treatment with IL-1β to chondrocytes for 24 hours. 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: 30μg/ml O3 improved the viability of chondrocytes. O3 significantly increased the level of autophagy proteins and the numbers of autophagosomes in chondrocytes treated with IL-1β via treated with O3. 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: 30μg/ml O3 improved autophagy via activating PPARγ/mTOR signaling and suppressing inflammation in chondrocytes treated with IL-1β.
Keywords
O3, Osteoarthritis, PPARγ/mTOR, Autophagy, Inflammation
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CURRENT STATUS: Under Revision
Version 1
Posted 13 Aug, 2020
No community comments so far
Editorial decision: Major revision
On 29 Dec, 2020
Review #2 received
Received 21 Sep, 2020
Review #1 received
Received 21 Sep, 2020
Reviewer #2 agreed
On 03 Sep, 2020
Reviewer #1 agreed
On 27 Aug, 2020
Reviewers invited
Invitations sent on 24 Aug, 2020
Editor assigned
On 31 Jul, 2020
Submission checks complete
On 30 Jul, 2020
Editor invited
On 30 Jul, 2020
First submitted
On 29 Jul, 2020
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Subject Areas
Orthopedics
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This preprint is under consideration at BMC Musculoskeletal Disorders. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Ozone Induces Autophagy by Activating PPARγ/mTOR in Rat Chondrocytes Treated with IL-1β
Zhijian Fu
Shandong Provincial Hospital
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Revision
Version 1
Posted 13 Aug, 2020
No community comments so far
Editorial decision: Major revision
On 29 Dec, 2020
Review #2 received
Received 21 Sep, 2020
Review #1 received
Received 21 Sep, 2020
Reviewer #2 agreed
On 03 Sep, 2020
Reviewer #1 agreed
On 27 Aug, 2020
Reviewers invited
Invitations sent on 24 Aug, 2020
Editor assigned
On 31 Jul, 2020
Submission checks complete
On 30 Jul, 2020
Editor invited
On 30 Jul, 2020
First submitted
On 29 Jul, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Orthopedics
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Osteoarthritis (OA) is the main cause of older pain and disability, its dysfunction due to discomfort as well as the quality of life of patients having adverse effects. Medical ozone (O3) has been found to have antioxidative and anti-inflammatory effects in the treatment of osteoarthritis. However, it is unclear whether O3 can induces autophagy through the PPARγ/mTOR autophagy pathway in chondrocytes treated with IL-1β.
Methods: Primary chondrocytes were isolated from wistar rat cartilage within 3days. The OA chondrocyte model was induced via treatment with IL-1β to chondrocytes for 24 hours. 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: 30μg/ml O3 improved the viability of chondrocytes. O3 significantly increased the level of autophagy proteins and the numbers of autophagosomes in chondrocytes treated with IL-1β via treated with O3. 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: 30μg/ml O3 improved autophagy via activating PPARγ/mTOR signaling and suppressing inflammation in chondrocytes treated with IL-1β.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6