Paeonol alleviates interleukin-1β-induced inflammatory responses in chondrocytes during osteoarthritis

Liu, Mingran; Shu-qiang, Zhong; Kong, Ruifeng; Shao, Hong; Wang, Chunyan; Piao, Hongying; Lv, Wentao; Chu, Xiaojie; Zhao, Yan

doi:10.1016/j.biopha.2017.09.011

Cited by 29 publications

(25 citation statements)

References 29 publications

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“…An increasing amount of evidence has shown that proliferation and apoptosis of chondrocytes play great roles in cartilage development, aging and disease [32]. Our results showed that IL-1β markedly decreased proliferation of chondrocytes, which were consistent with previous studies [33]. Furthermore, we found that PAK1 was involved in IL-1β-inhibited proliferation of chondrocytes.…”

Section: Discussionsupporting

confidence: 92%

Up-regulation of P21-activated kinase 1 in osteoarthritis chondrocytes is responsible for osteoarthritic cartilage destruction

Wang²,

Wang³

et al. 2020

Bioscience Reports

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Osteoarthritis is mainly caused by a degenerative joint disorder, which is characterized by the gradual degradation of articular cartilage and synovial inflammation. The chondrocyte, the unique resident cell type of articular cartilage, is crucial for the development of osteoarthritis. Previous studies revealed that P21-activated kinase-1 (PAK1) was responsible for the initiation of inflammation. The purpose of the present study was to determine the potential role of PAK1 in osteoarthritis. The level of PAK1 expression was measured by Western blot and quantitative real-time PCR in articular cartilage from osteoarthritis model rats and patients with osteoarthritis. In addition, the functional role of aberrant PAK1 expression was detected in the chondrocytes. We found that the expression of PAK1 was significantly increased in chondrocytes treated with osteoarthritis-related factors. Increased expression of PAK1 was also observed in knee articular cartilage samples from patients with osteoarthritis and osteoarthritis model rats. PAK1 was found to inhibit chondrocytes proliferation and to promote the production of inflammatory cytokines in cartilages chondrocytes. Furthermore, we found that PAK1 modulated the production of extracellular matrix and cartilage degrading enzymes in chondrocytes. Results of the present studies demonstrated that PAK1 might play an important role in the pathogenesis of osteoarthritis.

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Section: Discussionsupporting

confidence: 92%

Up-regulation of P21-activated kinase 1 in osteoarthritis chondrocytes is responsible for osteoarthritic cartilage destruction

Wang²,

Wang³

et al. 2020

Bioscience Reports

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“…Levels of ROS in BMMs and chondrocytes were measured using DCFH‐DA probe according to a previous study . BMMs were cultured with or without 50 ng/mL RANKL and 30 ng/mL M‐CSF as well as different concentrations of Iso for 24 hours.…”

Section: Methodsmentioning

confidence: 99%

“…The fluorescence signals were measured using confocal fluorescence imaging microscopy. Mitochondrial depolarization occurring during apoptosis could be indicated as an increase in the green/red fluorescence ratio …”

Section: Methodsmentioning

confidence: 99%

Isorhamnetin attenuates osteoarthritis by inhibiting osteoclastogenesis and protecting chondrocytes through modulating reactive oxygen species homeostasis

Zhou

Mei

Yuan

et al. 2019

J Cellular Molecular Medi

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Increasing evidence indicates that osteoarthritis (OA) is a musculoskeletal disease affecting the whole joint, including both cartilage and subchondral bone. Reactive oxygen species (ROS) have been demonstrated to be one of the important destructive factors during early‐stage OA development. The objective of this study was to investigate isorhamnetin (Iso) treatment on osteoclast formation and chondrocyte protection to attenuate OA by modulating ROS. Receptor activator of nuclear factor‐kappa B ligand (RANKL) was used to establish the osteoclast differentiation model in bone marrow macrophages (BMMs) in vivo. H 2 O 2 was used to induce ROS, which could further cause chondrocyte apoptosis. We demonstrated that Iso suppressed RANKL‐induced ROS generation, which could mediate osteoclastogenesis. Moreover, we found that Iso inhibited osteoclast formation and function by suppressing the expression of osteoclastogenesis‐related genes and proteins. We proved that Iso inhibited RANKL‐induced activation of mitogen‐activated protein kinase activation of mitogen‐activated protein kinase (MAPK), nuclear factor‐kappa B (NF‐κB) and AKT signalling pathways in BMMs. In addition, Iso inhibited ROS‐induced chondrocyte apoptosis by regulating apoptosis‐related proteins. Moreover, Iso was administered to an anterior cruciate ligament transection (ACLT)‐induced OA mouse model. The results indicated that Iso exerted beneficial effects on inhibiting excessive osteoclast activity and chondrocyte apoptosis, which further remedied cartilage damage. Overall, our data showed that Iso is an effective candidate for treating OA.

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“…currently available pharmacological treatments have failed to halt or reverse the progression of OA, and are accompanied by a variety of side effects (16). Thus, bioactive small molecules from natural herbage that may be suitable for OA treatment have recently been drawing attention, particularly those with minimal or no side effects (17)(18)(19). ART, a bioactive small molecule, has been used to treat various ailments ranging from malaria to tumors and RA (20).…”

Section: Discussionmentioning

confidence: 99%

Artesunate alleviates interleukin‑1β‑induced inflammatory response and apoptosis by inhibiting the NF‑κB signaling pathway in chondrocyte‑like ATDC5 cells, and delays the progression of osteoarthritis in a mouse model

Ren

et al. 2019

Int J Mol Med

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Osteoarthritis (OA) is a progressive and degenerative joint disorder that is highly prevalent worldwide and for which there is currently no effective medical therapy. Artesunate (ART), a natural compound used to treat malaria, possesses diverse biological properties, including the regulation of inflammation and apoptosis in various cells; however, its role in OA remains unclear. The aim of the present study was to investigate the effects of ART on interleukin (IL)-1β-induced chondrocyte-like ATdc5 cells and in an OA mouse model. The results revealed that ART dose-dependently relieved the inhibitory effect of IL-1β on cell viability. Moreover, ART significantly reduced the overexpression of matrix metalloproteinase (MMP)-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-5 and cyclooxygenase-2 at both the gene and protein levels in chondrocyte-like ATdc5 cells stimulated by IL-1β. Furthermore, ART decreased the expression of pro-apoptotic Bax, cleaved caspase-3 and cleaved caspase-7 in a dose-dependent manner, and increased the expression of the anti-apoptotic factor Bcl-2. These changes were mediated by the inhibitory effect of ART on the nuclear factor-κB signaling pathway, defined as repression of the phosphorylation of IκBα and p65, and improved redistribution of p65. Additionally, ART blocked the advancement of the calcified cartilage zone and the loss of proteoglycan, and lowered histological scoring of OA in a mouse model. Taken together, these results indicate that ART may be of value as a therapeutic agent for OA.

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Paeonol alleviates interleukin-1β-induced inflammatory responses in chondrocytes during osteoarthritis

Cited by 29 publications

References 29 publications

Up-regulation of P21-activated kinase 1 in osteoarthritis chondrocytes is responsible for osteoarthritic cartilage destruction

Up-regulation of P21-activated kinase 1 in osteoarthritis chondrocytes is responsible for osteoarthritic cartilage destruction

Isorhamnetin attenuates osteoarthritis by inhibiting osteoclastogenesis and protecting chondrocytes through modulating reactive oxygen species homeostasis

Artesunate alleviates interleukin‑1β‑induced inflammatory response and apoptosis by inhibiting the NF‑κB signaling pathway in chondrocyte‑like ATDC5 cells, and delays the progression of osteoarthritis in a mouse model

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