Ozone Induces Autophagy by Activating PPARγ/mTOR in Rat Chondrocytes Treated with IL-1β
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.
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Posted 13 Aug, 2020
On 29 Dec, 2020
Received 21 Sep, 2020
Received 21 Sep, 2020
On 03 Sep, 2020
On 27 Aug, 2020
Invitations sent on 24 Aug, 2020
On 31 Jul, 2020
On 30 Jul, 2020
On 30 Jul, 2020
On 29 Jul, 2020
Ozone Induces Autophagy by Activating PPARγ/mTOR in Rat Chondrocytes Treated with IL-1β
Posted 13 Aug, 2020
On 29 Dec, 2020
Received 21 Sep, 2020
Received 21 Sep, 2020
On 03 Sep, 2020
On 27 Aug, 2020
Invitations sent on 24 Aug, 2020
On 31 Jul, 2020
On 30 Jul, 2020
On 30 Jul, 2020
On 29 Jul, 2020
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