&lt;p&gt;Tanshinone I Inhibits IL-1β-Induced Apoptosis, Inflammation And Extracellular Matrix Degradation In Chondrocytes CHON-001 Cells And Attenuates Murine Osteoarthritis&lt;/p&gt;

Fan, Jiyang; Ding, Xinyu; Sun, Yuyu; Cui, Zhiming; Liu, Wei

doi:10.2147/dddt.s216596

Cited by 63 publications

(48 citation statements)

References 46 publications

(48 reference statements)

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“…The present study demonstrated that MIR4435-2HG was significantly downregulated in IL-1β-treated CHON-001 cells. Similarly, Wang et al ( 16 ) indicated that the expression of lncRNA-recombination signal binding protein for immunoglobulin κ J region (RBPJ, previously known as CBF1) interacting corepressor displayed an inhibitory role during OA progression. In addition, a recent study reported that the inflammatory response plays an important role during the progression of OA ( 23 ).…”

Section: Discussionmentioning

confidence: 99%

“…Cells were cultured in RPMI-1640 medium (Invitrogen; Thermo Fisher Scientific, Inc.) supplemented with 10% fetal bovine serum (Invitrogen; Thermo Fisher Scientific, Inc.) and 2 mM glutamine (Sigma-Aldrich; Merck KGaA) andplaced at 37˚C in a humidified incubator containing 5% CO 2 . CHON-001 cells were treated with 10 ng/ml interleukin (IL)-1β (Sigma-Aldrich; Merck KGaA) at room temperaturefor 24 h to generate an in vitro model of OA ( 16 ). The nuclear factor κB (NF-κB) inhibitor BAY 11-7085 (10 µM) was purchased from MedChemExpress.…”

Section: Methodsmentioning

confidence: 99%

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LncRNA MIR4435‑2HG inhibits the progression of osteoarthritis through miR‑510‑3p sponging

et al. 2020

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Osteoarthritis (OA) is a disorder of diarthrodial joints that can have multiple causes. Long non-coding RNAs (lncRNAs) participate in multiple diseases, including OA. It has recently been reported that the lncRNA microRNA 4435-2HG (MIR4435-2HG) is downregulated in OA tissues; however, the biological role of MIR4435-2HG during OA progression remains unclear. In the present study, interleukin (IL)-1β was used to establish an in vitro model of OA. Protein expressions of matrix metallopeptidase (MMP) 1, MMP13, collagen II, interleukin (IL)-17A, p65, phosphorylated (p)-p65, IκB and p-IκB in CHON-001 cells were detected by western blotting. Gene expressions of IL-17A, MIR4435-2HG and miR-510-3p in tissues or CHON-001 cells were measured by reverse transcription-quantitative PCR and western blotting, respectively. Cell Counting Kit-8 assay and immunofluorescence staining were used to investigate cell proliferation, and cell apoptosis was detected by flow cytometry. The association between MIR4435-2HG, miR-510-3p and IL-17A was investigated using the dual luciferase report assay. MIR4435-2HG and miR-510-3p overexpression were transfected into CHON-001 cells. The results demonstrated that miR4435-2HG overexpression significantly increased proliferation and inhibited apoptosis of CHON-001 cells. In addition, miR-510-3p was identified as the downstream target of MIR4435-2HG, and miR-510-3p directly targeted IL-17A. The results from the present study suggested that MIR4435-2HG could mediate the progression of OA by inactivating the NF-κB signaling pathway. In addition, miR4435-2HG overexpression inhibited OA progression, suggesting that miR4435-2HG may be considered as a potential therapeutic target in OA.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

LncRNA MIR4435‑2HG inhibits the progression of osteoarthritis through miR‑510‑3p sponging

et al. 2020

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“…8 It has been found in the research of joint diseases that caspase-1 is one of the risk factors for osteoarthritis and accelerated cartilage destruction. 38 In this work, our team sought to investigate the antiinflammatory mechanism of Chrysin in vitro and in vivo by targeting the NLRP3 inflammasome. First, CCK-8 was performed to investigate the effect of Chrysin at different concentrations on the cytotoxicity of FLS, and 5 ug/mL Chrysin exhibited no cytotoxicity.…”

Section: Discussionmentioning

confidence: 99%

<p>Chrysin Attenuates the NLRP3 Inflammasome Cascade to Reduce Synovitis and Pain in KOA Rats</p>

Liao

Ding

et al. 2020

DDDT

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Our recent reports have revealed that inhibiting NLRP3 activation reduces synovial inflammation and fibrosis in knee osteoarthritis (KOA). Synovial inflammation is involved the entire process of KOA and promotes the progression of KOA. Natural flavonoid Chrysin from Scutellariae Radix, a traditional Chinese medicine, exhibits multifarious biological activities and potentially has protective activity against osteoarthritis. However, the mechanism of Chrysin in the treatment of synovial inflammation remains elusive. The purpose of our research was to explore the anti-inflammatory effects of Chrysin on KOA, which was induced by monoiodoacetic acid (MIA) in rats by targeting the NLRP3 inflammasome in the hopes of identifying an effective drug to treat KOA. Methods: The MIA-induced KOA model was used to evaluate the cold pain threshold and paw withdrawal threshold (PWT) of joints after MIA (40 mg/mL) injection into the knee joints. Microscopically, we used LPS (5 ug/mL) and ATP (4 mmol/L) to stimulate fibroblast-like synovial cells (FLSs) to explore the underlying mechanisms and effects of Chrysin. Two staining methods, H&E and Sirius Red, were applied to assess histopathological changes in synovial membranes. Cellular signal transduction was determined by qRT-PCR and WB. Cytokine expression (inflammatory cytokines and pain-related cytokines) was detected by ELISA. The degree of chronic inflammatory pain was evaluated by c-Fos immunofluorescence. Results: The results showed that Chrysin not only attenuated synovial inflammation but also reduced the secretion of pain-related factors and increased the PWT and cold pain threshold in rats. Chrysin also inhibited NLRP3 inflammasome activation and increased IL-1β levels to alleviate the synovitis. Conclusion: Chrysin can relieve knee synovial inflammation and improve pain behavior in KOA rats, which may be related to the ability of Chrysin to inhibit NLRP3 inflammasome activation. Therefore, Chrysin may be developed as a new drug for the treatment of KOA.

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“…Collagen II and MMPs are potential targets for the treatment of OA. Inhibition of Collagen II degradation reduces the pathological changes of OA [ 29 ]. Inhibition of MMP-13 activity maintains the extracellular matrix structure of cartilage and reduces morphological damage [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Platelet-Rich Plasma Combined with Alendronate Reduces Pain and Inflammation in Induced Osteoarthritis in Rats by Inhibiting the Nuclear Factor-Kappa B Signaling Pathway

Xin

Wang

Yuan

et al. 2020

BioMed Research International

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Purpose. Osteoarthritis (OA) is one of the common degenerative diseases of the joint in the world. This study was designed to explore the effect of platelet-rich plasma (PRP) combined with alendronate (ALN) on OA. Methods. We induced OA model by anterior cruciate ligament transection (ACLT) method in rats and treating chondrocytes by IL-1β in vitro. PRP and/or ALN were used to treat induced rats and chondrocytes. Hematoxylin and eosin (H&E) and Safranin O staining were used to observe the structures of cartilage. The mRNA expression of Collagen II, MMP-13, and inflammatory factors (IL-18, IL-1β, and TNF-α) in the cartilage and chondrocytes of rats was determined by qRT-PCR. The expression of NF-κB pathway-related proteins (p-p65, p65, IκBα, and p-IκBα) in the cartilage and chondrocytes of rats was determined by Western blot. The proliferation of chondrocytes was detected by MTT assay. Results. Treatment with PRP, ALN, or PRP combined with ALN decreased the degree of cartilage destruction, the mRNA expression of MMP-13 and inflammatory factors (IL-18, IL-1β, and TNF-α), and the protein expression of p-IκBα/IκBα and p-p65/p65, increased Collagen II expression, and the threshold of tender and thermal pain in OA rats. Meanwhile, ALN, PRP, or ALN combined with PRP reversed the inhibiting effect of phorbol myristate acetate (PMA, an NF-κB agonist) on cell proliferation and cartilage matrix metabolism. Among them, the effects of ALN combined with PRP were most obvious. Conclusion. PRP combined with ALN delayed OA progression by inhibiting the NF-κB signaling pathway.

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<p>Tanshinone I Inhibits IL-1β-Induced Apoptosis, Inflammation And Extracellular Matrix Degradation In Chondrocytes CHON-001 Cells And Attenuates Murine Osteoarthritis</p>

Cited by 63 publications

References 46 publications

LncRNA MIR4435‑2HG inhibits the progression of osteoarthritis through miR‑510‑3p sponging

LncRNA MIR4435‑2HG inhibits the progression of osteoarthritis through miR‑510‑3p sponging

<p>Chrysin Attenuates the NLRP3 Inflammasome Cascade to Reduce Synovitis and Pain in KOA Rats</p>

Platelet-Rich Plasma Combined with Alendronate Reduces Pain and Inflammation in Induced Osteoarthritis in Rats by Inhibiting the Nuclear Factor-Kappa B Signaling Pathway

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