Aucubin prevents interleukin-1 beta induced inflammation and cartilage matrix degradation via inhibition of NF-κB signaling pathway in rat articular chondrocytes

Wang, Shengnan; Xie, Gary; Qin, Chenghe; Chen, Yirong; Zhang, Kai-rui; Li, Xue; Qian, Wei; Dong, Wei; Yang, Jun; Yu, Bin

doi:10.1016/j.intimp.2014.12.029

Cited by 84 publications

(62 citation statements)

References 27 publications

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“…IL-1β has been regarded as a classic pro-inflammatory and pro-catabolic factor in chondrocytes, contributing to the degradation of ECM [25, 26]. The present study also showed that IL-1β increased the expression of COX-2, PGE2, and iNOS which was an enzyme producing NO.…”

Section: Discussionsupporting

confidence: 76%

“…The present study also showed that IL-1β increased the expression of COX-2, PGE2, and iNOS which was an enzyme producing NO. COX-2 and PGE2 are the primary mediators of osteoarthritis pain induced by inflammation [26]. The in vitro studies demonstrated that PTE could inhibit the expression of these inflammatory mediators induced by IL-1β, suggesting it as a candidate to relieve the pain symptom of OA.…”

Section: Discussionmentioning

confidence: 99%

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Pterostilbene inhibits inflammation and ROS production in chondrocytes by activating Nrf2 pathway

Xue

Lin²,

Zhang

et al. 2017

Oncotarget

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Pterostilbene has been reported as a potential drug to inhibit oxidative stress and inflammation. However, the effect of pterostilbene on chondrocytes and osteoarthritis remains to be elucidated. We sought to investigate whether pterostilbene could protect chondrocytes from inflammation and ROS production through factor erythroid 2-related factor 2 (Nrf2) activation. The pterostilbene toxicity on chondrocytes collected from cartilages of Sprague-Dawley rats was assessed by CCK-8 test. Immunofluorescence and Western blotting explored the nuclear translocation of Nrf2. Nrf2 expression was silenced by siRNA to evaluate the involvement of Nrf2 in the effect of pterostilbene on chondrocytes. Finally, osteoarthritis model was established by the transection of anterior cruciate ligament and partial medial meniscectomy in rats, and then these rats received pterostilbene 30 mg/kg, daily, p.o. for 8 weeks. Histology and immunohistochemistry were used to assess histopathological change and Nrf2 expression in cartilage. Nuclear translocation of Nrf2 was stimulated by pterostilbene without cellular toxicity. Pterostilbene inhibited the level of COX-2, iNOS, PGE2, and NO, as well as the mitochondrial and total intracellular ROS production induced by IL-1β in chondrocytes, partially reversed by the Nrf2 silencing. Pterostilbene prevented cartilage degeneration and promoted the nuclear translocation of Nrf2 in cartilage. These results suggest that pterostilbene could inhibit the IL-1β-induced inflammation and ROS production in chondrocytes by stimulating the nuclear translocation of Nrf2.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Pterostilbene inhibits inflammation and ROS production in chondrocytes by activating Nrf2 pathway

Xue

Lin²,

Zhang

et al. 2017

Oncotarget

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“…The NF-κB dimer therefore locates mainly in the nucleus where it binds to specific sites in the promoter regions of sensitive genes and promotes transcription (122). NF-κB transcription factors can be triggered by a host of stress-related stimuli like pro-inflammatory cytokines IL-1 (123); indeed, through the canonical NF-κB pathway to trigger the expression of metalloproteinases (MMPs), prostaglandin E2 (PGE2), nitric oxide (NO), and type X collagen in chondrocytes (124,125), leading to increased cartilage degradation and chondrocyte hypertrophy in OA cartilage.…”

Section: Role Of Inflammatory Signal Nf-κb In Oamentioning

confidence: 99%

Recent advances in the understanding of molecular mechanisms of cartilage degeneration, synovitis and subchondral bone changes in osteoarthritis

Wei

Bai

2016

Connective Tissue Research

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Osteoarthritis (OA), the most common form of degenerative joint disease, is linked to high morbidity. It is predicted to be the single greatest cause of disability in the general population by 2030. The development of disease-modifying therapy for OA currently face great obstacle mainly because the onset and development of the disease involve complex molecular mechanisms. In this review, we will comprehensively summarize biological and pathological mechanisms of three key aspects: degeneration of articular cartilage, synovial immunopathogenesis, and changes in subchondral bone. For each tissue, we will focus on the molecular receptors, cytokines, peptidases, related cell, and signal pathways. Agents that specifically block mechanisms involved in synovial inflammation, degeneration of articular cartilage, and subchondral bone remodeling can potentially be exploited to produce targeted therapy for OA. Such new comprehensive agents will benefit affected patients and bring exciting new hope for the treatment of OA.

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“…The upstream targets of iNOS expression are associated with three main regulators including NF-kB, STAT-1 and MAPKs signaling pathways [21]. More specifically, IL-1b-induced OA is mainly associated with translocation of NF-kB into nucleus, where it binds to the promotor region of iNOS [22]. Subsequently, iNOS efficiently catalyzes the production of nitric oxide (NO) which plays a critical role in the pathogenesis of OA [23].…”

Section: Discussionmentioning

confidence: 99%

Foxo3a aggravates inflammation and induces apoptosis in IL-1-treated rabbit chondrocytes via positively regulating tenascin-c

Wang

Qiu-bin

Zhu

et al. 2020

Folia Histochem Cytobiol.

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Introduction. Osteoarthritis (OA) is the most common degenerative disease in middle-aged and elderly individuals that causes joint deformity and limb disability. Accumulating evidence has suggested that the pathogenesis of OA has been related to various mechanisms such as apoptosis, inflammation, oxidative stress and metabolic disorders. The aim of this study is to clarify the role of Foxo3a in the progress of OA in an in vitro model. Materials and methods. The chondrocytes were derived from rabbit, and treated with IL-1b, which was used as an in vitro OA model. The over-expression and down-regulation of Foxo3a were achieved by transfection with overexpression vector or shRNA, respectively. The mRNA level of iNOS in chondrocytes was quantified by qPCR. Tenascin-c (Tnc) production was measured by ELISA and apoptosis-associated proteins were analyzed by Western blotting. The MTT assay was used to assess the viability of chondrocytes. Results. Foxo3a and iNOS expression were upregulated in IL-1b-treated chondrocytes. Foxo3a silencing decreased iNOS expression, and inhibited apoptosis of IL-1b-treated chondrocytes. The production of Tnc was significantly increased in IL-1b-treated chondrocytes and was positively regulated by Foxo3. Importantly, extracellular addition of Tnc abrogated the protective effects of Foxo3a knockdown on IL-1b -treated chondrocytes. Conclusion. The present study indicated that down-regulation of Foxo3a protected IL-1b-treated chondrocytes by decreasing iNOS expression and suppressing chondrocytes' apoptosis via modulating tenascin-c, which could be regarded as a potent therapeutic target for the treatment of OA.

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Aucubin prevents interleukin-1 beta induced inflammation and cartilage matrix degradation via inhibition of NF-κB signaling pathway in rat articular chondrocytes

Cited by 84 publications

References 27 publications

Pterostilbene inhibits inflammation and ROS production in chondrocytes by activating Nrf2 pathway

Pterostilbene inhibits inflammation and ROS production in chondrocytes by activating Nrf2 pathway

Recent advances in the understanding of molecular mechanisms of cartilage degeneration, synovitis and subchondral bone changes in osteoarthritis

Foxo3a aggravates inflammation and induces apoptosis in IL-1-treated rabbit chondrocytes via positively regulating tenascin-c

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