Oridonin inhibits IL-1β-induced inflammation in human osteoarthritis chondrocytes by activating PPAR-γ

Jia, Ting; Cai, Mengmeng; Ma, Xu; Li, Ming; Jian, Qiao; Chen, Tianxin

doi:10.1016/j.intimp.2019.01.049

Cited by 28 publications

(21 citation statements)

References 28 publications

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“…Considering that O 3 blocked IL-1βinduced autophagy inhibition in chondrocytes, the result is likely due to its anti-in ammatory effect on chondrocytes. Moreover, studies have shown that IL-1β can induce the expression of MMPs, in turn inducing cartilage matrix degradation [35]. The result of qRT-PCR results revealed that the levels of MMP-13 and MMP-3 were decreased with O 3 treatment.…”

Section: Discussionmentioning

confidence: 92%

Ozone Induces Autophagy by Activating PPARγ/mTOR in Rat Chondrocytes Treated with IL-1β

Sun

Zhang

et al. 2020

Preprint

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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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Section: Discussionmentioning

confidence: 92%

Ozone Induces Autophagy by Activating PPARγ/mTOR in Rat Chondrocytes Treated with IL-1β

Sun

Zhang

et al. 2020

Preprint

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“…Inflammatory bone loss with high expression of IL1β is a common finding in clinical settings, such as osteoarthritis 31 and rheumatoid arthritis, 32 also including alveolar bone loss caused by periodontitis 33 and cementum loss due to orthodontic root resorption. 34 As two of the most important inflammatory factors, TNF-α and IL1β had some different reactions in miRNA-mediated in inflammatory diseases.…”

Section: Discussionmentioning

confidence: 99%

IL1β inhibits differentiation of cementoblasts via microRNA‐325‐3p

Wang

Shao

et al. 2019

J of Cellular Biochemistry

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Cementum regeneration is considered the gold standard for the treatment of periodontitis. As one of the most important primary proinflammatory cytokines, interleukin 1β (IL1β) plays an essential role during the early stage of periodontitis and its amounts simultaneously increase dramatically during this stage. Though promising, the differentiation of cementoblasts upon IL1β-induced inflammation of the microenvironment and the relative interaction mechanism are still unknown.Here, we found that IL1β inhibited cementoblast differentiation and microRNA-325-3p (miR-325-3p) was increased during IL1β-stimulated cementoblasts. Bioinformatics analysis and luciferase reporter assay demonstrated miR-325-3p targeted runt-related transcription factor 2 directly. Transfection of miR-325-3p suppressed cementoblast differentiation in vitro and the formation of cementum-like tissues in vivo. The inhibitor of miR-325-3p could mitigate the above effects induced by IL1β. Accordingly, our finding suggests a critical role of miR-325-3p in linking inflammation to impaired cementum regeneration and provides a potential possibility for applying miR-325-3p inhibitors in the treatment of periodontitisrelated bone loss.

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“…Присутствие синовита, даже субклинического, приводит к повышению уровня ряда ключевых провоспалительных цитокиновинтерлейкинов 1, 6, 8, 15, фактора некроза опухоли (ФНО) альфа, которые поддерживают воспаление и способствуют развитию катаболических процессов в суставном хряще и субхондральной кости [9]. По данным T. Jia и соавт., при ОА в хондроцитах человека повышается концентрация интерлейкина 1-бета, а также индуцированная интерлейкином 1-бета продукция металлопротеиназ 1, 3 и 13, оксида азота и простагландина Е2 [10]. Аналогичные данные выявлены и в экспериментальных моделях ОА [11,12].…”

Section: патогенезunclassified

Use of Non-Steroidal Anti-Inflammatory Drugs in Osteoarthritis: a Sight Through the Prism of Pathogenesis

Zaytseva¹,

Kuzin²

2019

EPh

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Oridonin inhibits IL-1β-induced inflammation in human osteoarthritis chondrocytes by activating PPAR-γ

Cited by 28 publications

References 28 publications

Ozone Induces Autophagy by Activating PPARγ/mTOR in Rat Chondrocytes Treated with IL-1β

Ozone Induces Autophagy by Activating PPARγ/mTOR in Rat Chondrocytes Treated with IL-1β

IL1β inhibits differentiation of cementoblasts via microRNA‐325‐3p

Use of Non-Steroidal Anti-Inflammatory Drugs in Osteoarthritis: a Sight Through the Prism of Pathogenesis

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