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Title:
Resveratrol alleviates the interleukin-1β-induced chondrocytes injury through the NF-κB signaling pathway | Journal of Orthopaedic Surgery and Research
Description:
Background Osteoarthritis (OA) is a regular age-related disease that affects millions of people. Resveratrol (RSV) is a flavonoid with a stilbene structure with different pharmacological effects. The purpose of the experiment was to evaluate the protective role of RSV against the human OA chondrocyte injury induced by interleukin-1β (IL-1β). Methods Chondrocytes were isolated from OA patients and identified by type II collagen, safranin O staining, and toluidine blue staining. Differentially expressed genes in chondrocytes treated RSV were identified by RNA sequencing. Kyoto encyclopedia of genes and genomes (KEGG) pathway as well as gene ontology (GO) were further conducted through Metascape online tool. A cell counting kit-8 (CCK-8) assay was applied to discover the viability of chondrocytes (6, 12, 24, and 48āμM). Many genes associated with inflammation and matrix degradation are evaluated by real-time PCR (RT-PCR) as well as western blot (WB). The mechanism of RSV for protecting IL-1β induced chondrocytes injury was further measured through immunofluorescence and WB assays. Results A total of 845 differentially expressed genes (upregulated = 499, downregulated = 346) were found. These differentially expressed genes mainly enriched into negative regulation of catabolic process, autophagy, and cellular catabolic process, intrinsic apoptotic, apoptotic, and regulation of apoptotic signaling pathway, cellular response to abiotic stimulus, external stimuli, stress, and radiation. These differentially expressed genes were obviously enriched in NF-kB signaling pathway. RSV at the concentration of 48āμM markedly weakened the viability of the cells after 24āh of treatment (87% vs 100%, P < 0.05). No obvious difference was observed between the 6, 12, and 24āμM groups (106% vs 100%, 104% vs 100%, 103% vs 100%, P > 0.05). RSV (24āμM) also markedly depressed the levels of PGE2 and NO induced by IL-1β by 25% and 29% respectively (P < 0.05). Our experiment pointed out that RSV could dramatically inhibit the inflammatory response induced by IL-1β, including the MMP-13, MMP-3, and MMP-1 in human OA chondrocytes by 50%, 35%, and 33% respectively. On the other hand, RSV inhibited cyclooxygenase-2 (COX-2), matrix metalloproteinase-1 (MMP-1), MMP-3, MMP-13, and inducible nitric oxide synthase (iNOs) expression (P < 0.05), while increased collagen-II and aggrecan levels (P < 0.05). From a mechanistic perspective, RSV inhibited the degradation of IĪŗB-α as well as the activation of nuclear factor-kappa B (NF-ĪŗB) induced by IL-1β. Conclusion In summary, RSV regulates the signaling pathway of NF-ĪŗB, thus inhibiting inflammation and matrix degradation in chondrocytes. More studies should be focused on the treatment efficacy of RSV for OA in vivo.
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Keywords {š}
rsv, chondrocytes, pathway, signaling, ilβ, article, mmp, genes, nfκb, osteoarthritis, google, scholar, resveratrol, response, expression, fig, differentially, expressed, inflammation, cas, human, induced, cell, study, inflammatory, cartilage, analysis, zhang, articular, rna, gene, regulation, data, sequencing, matrix, degradation, found, treatment, effects, results, groups, progression, research, wei, type, staining, treated, pge, control, knee,
Topics {āļø}
suppressing pi3k/akt/nf-κb pathway malat1/mir-9/nf-κb signaling pathway suppressing pi3k/akt/nuclear factor-kappa nrf2/ho-1/nf-κb signaling pathway nf-kappab signalling pathway p38/nf-kb-dependent expression pi3k/akt signaling pathways interleukin-1β-induced chondrocytes injury nf-kappab signaling pathway nf-kb signaling pathway nf-κb signaling pathway nf-κb signaling overactivation regular age-related disease nucleus pulposus cell-mediated il-1β-induced chondrocytes inflammation platelet-rich plasma injection nf-κb signaling plays cytokine-cytokine receptor interaction affecting nuclear factor-kappa il-1α-challenged chondrocytes article download pdf il-1beta-induced expression double-stranded cdna purified nf-κb p65 dissociates large-scale meta-analysis human chondrocyte cultures il-1β stimulation increases full access bayesian network meta-analysis nf-kappab pathway underlying molecular mechanisms nf-κb pathway /nf-κb pathway collagen-ii expression level il-1β-induced pge2 real-time pcr privacy choices/manage cookies il-17 signaling pathway il-1β dramatically increased human osteoarthritis chondrocytes sybr green premix rheumatoid arthritis nf-κb bounded human articular chondrocytes arthritis res ther top ten enriched apoptotic signaling pathway platelet-rich plasma anti-inflammatory mechanisms type ii collagen
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headline:Resveratrol alleviates the interleukin-1β-induced chondrocytes injury through the NF-κB signaling pathway
description:Osteoarthritis (OA) is a regular age-related disease that affects millions of people. Resveratrol (RSV) is a flavonoid with a stilbene structure with different pharmacological effects. The purpose of the experiment was to evaluate the protective role of RSV against the human OA chondrocyte injury induced by interleukin-1β (IL-1β). Chondrocytes were isolated from OA patients and identified by type II collagen, safranin O staining, and toluidine blue staining. Differentially expressed genes in chondrocytes treated RSV were identified by RNA sequencing. Kyoto encyclopedia of genes and genomes (KEGG) pathway as well as gene ontology (GO) were further conducted through Metascape online tool. A cell counting kit-8 (CCK-8) assay was applied to discover the viability of chondrocytes (6, 12, 24, and 48āμM). Many genes associated with inflammation and matrix degradation are evaluated by real-time PCR (RT-PCR) as well as western blot (WB). The mechanism of RSV for protecting IL-1β induced chondrocytes injury was further measured through immunofluorescence and WB assays. A total of 845 differentially expressed genes (upregulated = 499, downregulated = 346) were found. These differentially expressed genes mainly enriched into negative regulation of catabolic process, autophagy, and cellular catabolic process, intrinsic apoptotic, apoptotic, and regulation of apoptotic signaling pathway, cellular response to abiotic stimulus, external stimuli, stress, and radiation. These differentially expressed genes were obviously enriched in NF-kB signaling pathway. RSV at the concentration of 48āμM markedly weakened the viability of the cells after 24āh of treatment (87% vs 100%, P < 0.05). No obvious difference was observed between the 6, 12, and 24āμM groups (106% vs 100%, 104% vs 100%, 103% vs 100%, P > 0.05). RSV (24āμM) also markedly depressed the levels of PGE2 and NO induced by IL-1β by 25% and 29% respectively (P < 0.05). Our experiment pointed out that RSV could dramatically inhibit the inflammatory response induced by IL-1β, including the MMP-13, MMP-3, and MMP-1 in human OA chondrocytes by 50%, 35%, and 33% respectively. On the other hand, RSV inhibited cyclooxygenase-2 (COX-2), matrix metalloproteinase-1 (MMP-1), MMP-3, MMP-13, and inducible nitric oxide synthase (iNOs) expression (P < 0.05), while increased collagen-II and aggrecan levels (P < 0.05). From a mechanistic perspective, RSV inhibited the degradation of IĪŗB-α as well as the activation of nuclear factor-kappa B (NF-ĪŗB) induced by IL-1β. In summary, RSV regulates the signaling pathway of NF-ĪŗB, thus inhibiting inflammation and matrix degradation in chondrocytes. More studies should be focused on the treatment efficacy of RSV for OA in vivo.
datePublished:2020-09-18T00:00:00Z
dateModified:2020-09-18T00:00:00Z
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license:http://creativecommons.org/publicdomain/zero/1.0/
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keywords:
Osteoarthritis
Resveratrol
MMP-3
MMP-13
MMP-1
NF-ĪŗB signaling pathway
Orthopedics
Surgical Orthopedics
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headline:Resveratrol alleviates the interleukin-1β-induced chondrocytes injury through the NF-κB signaling pathway
description:Osteoarthritis (OA) is a regular age-related disease that affects millions of people. Resveratrol (RSV) is a flavonoid with a stilbene structure with different pharmacological effects. The purpose of the experiment was to evaluate the protective role of RSV against the human OA chondrocyte injury induced by interleukin-1β (IL-1β). Chondrocytes were isolated from OA patients and identified by type II collagen, safranin O staining, and toluidine blue staining. Differentially expressed genes in chondrocytes treated RSV were identified by RNA sequencing. Kyoto encyclopedia of genes and genomes (KEGG) pathway as well as gene ontology (GO) were further conducted through Metascape online tool. A cell counting kit-8 (CCK-8) assay was applied to discover the viability of chondrocytes (6, 12, 24, and 48āμM). Many genes associated with inflammation and matrix degradation are evaluated by real-time PCR (RT-PCR) as well as western blot (WB). The mechanism of RSV for protecting IL-1β induced chondrocytes injury was further measured through immunofluorescence and WB assays. A total of 845 differentially expressed genes (upregulated = 499, downregulated = 346) were found. These differentially expressed genes mainly enriched into negative regulation of catabolic process, autophagy, and cellular catabolic process, intrinsic apoptotic, apoptotic, and regulation of apoptotic signaling pathway, cellular response to abiotic stimulus, external stimuli, stress, and radiation. These differentially expressed genes were obviously enriched in NF-kB signaling pathway. RSV at the concentration of 48āμM markedly weakened the viability of the cells after 24āh of treatment (87% vs 100%, P < 0.05). No obvious difference was observed between the 6, 12, and 24āμM groups (106% vs 100%, 104% vs 100%, 103% vs 100%, P > 0.05). RSV (24āμM) also markedly depressed the levels of PGE2 and NO induced by IL-1β by 25% and 29% respectively (P < 0.05). Our experiment pointed out that RSV could dramatically inhibit the inflammatory response induced by IL-1β, including the MMP-13, MMP-3, and MMP-1 in human OA chondrocytes by 50%, 35%, and 33% respectively. On the other hand, RSV inhibited cyclooxygenase-2 (COX-2), matrix metalloproteinase-1 (MMP-1), MMP-3, MMP-13, and inducible nitric oxide synthase (iNOs) expression (P < 0.05), while increased collagen-II and aggrecan levels (P < 0.05). From a mechanistic perspective, RSV inhibited the degradation of IĪŗB-α as well as the activation of nuclear factor-kappa B (NF-ĪŗB) induced by IL-1β. In summary, RSV regulates the signaling pathway of NF-ĪŗB, thus inhibiting inflammation and matrix degradation in chondrocytes. More studies should be focused on the treatment efficacy of RSV for OA in vivo.
datePublished:2020-09-18T00:00:00Z
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Osteoarthritis
Resveratrol
MMP-3
MMP-13
MMP-1
NF-ĪŗB signaling pathway
Orthopedics
Surgical Orthopedics
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