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  1. Analyzed Page
  2. Matching Content Categories
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We began analyzing https://link.springer.com/article/10.1007/s12263-010-0179-5, but it redirected us to https://link.springer.com/article/10.1007/s12263-010-0179-5. The analysis below is for the second page.

Title[redir]:
Curcumin synergizes with resveratrol to stimulate the MAPK signaling pathway in human articular chondrocytes in vitro | Genes & Nutrition
Description:
The mitogen-activated protein kinase (MAPK) pathway is stimulated in differentiated chondrocytes and is an important signaling cascade for chondrocyte differentiation and survival. Pro-inflammatory cytokines such as interleukin 1β (IL-1β) play important roles in the pathogenesis of osteoarthritis (OA) and rheumatoid arthritis (RA). In this study, we investigated whether curcumin and resveratrol can synergistically inhibit the catabolic effects of IL-1β, specifically the inhibition of the MAPK and subsequent apoptosis in human articular chondrocytes. Chondrocytes were either left untreated or treated with 10 ng/ml IL-1β or 1 μM U0126, a specific inhibitor of MAPK pathway alone for the indicated time periods or pre-treated with 10 μM curcumin, 10 μM resveratrol or 10 μM resveratrol and 10 μM curcumin for 4 h followed by co-treatment with 10 ng/ml IL-1β or 1 μM U0126 and 10 μM resveratrol, 10 μM curcumin or 10 μM resveratrol and 10 μM curcumin for the indicated time periods. Cultures were evaluated by immunoblotting and transmission electron microscopy. Incubation of chondrocytes with IL-1β resulted in induction of apoptosis, downregulation of β1-integrins and the extracellular signal-regulated kinase 1/2 (Erk1/2). Interestingly, U0126 induced apoptosis and blocked the above-mentioned proteins in a similar way to IL-1β. Furthermore, curcumin and resveratrol inhibited IL-1β- or U0126-induced apoptosis and downregulation of β1-integrins and Erk1/2 in human articular chondrocytes. These results suggest that combining these two natural compounds activates MEK/Erk signaling, a pathway that is involved in the maintenance of chondrocyte differentiation and survival.

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Keywords {🔍}

curcumin, chondrocytes, resveratrol, google, scholar, article, pubmed, cas, ilβ, human, apoptosis, pathway, erk, inhibition, cell, mapk, articular, effects, activation, expression, fig, signaling, kinase, chondrocyte, cells, shakibaei, uinduced, cartilage, shown, caspase, serumstarved, osteoarthritis, matrix, ngml, treatment, nuclear, apoptotic, analysis, vitro, arthritis, specific, antibodies, andor, germany, mobasheri, protein, differentiation, cytokines, sox, transcription,

Topics {✒️}

il-1beta-induced nf-kappab-mediated inflammation il-1beta-stimulated c-28/i2 chondrocytes pkcdelta/jnk/c-jun pathway nuclear factor-kappab-regulated antiapoptotic ras-mitogen-activated kinase leads matrix-degrading gene products nf-kappab transcription factors il-1β-stimulated human chondrocytes nf-kappab mediates inhibition il-1β-mediated cellular responses deficient shc-erk interaction multi-functional β1-integrins [12] chondrocyte-specific marker genes 25 μg/ml ascorbic acid ameliorate collagen-induced arthritis tumor necrosis factor-alpha nf-κb-dependent pathway mitogen-activated protein kinase serum-starved human chondrocytes mouse limb-bud chondrocytes anti-β1-integrin antibodies phospho-p42/p44 erk1/2 cartilage-specific pericellular matrix il-1β-induced inhibition anti-pan erk1/2 antibody il-1β-induced apoptosis anti-pan erk1/2 antibodies 10 ng/ml il-1β cytokine-mediated chondrocyte apoptosis anti-phospho erk1/2 antibodies ludwig-maximilians-university munich pro-inflammatory cytokines marked dose-dependent increase inflammation gene products nuclear factor-kappab nf-kappab activation anti-phospho erk1/2 recognizes author information authors regulate gene expression nf-κb pathway privacy choices/manage cookies resveratrol inhibited il-1β curcumin block il-1β related subjects lin-shiau sy mitogen-activated protein serum-starved chondrocytes serum-starved medium anti-inflammatory functions [14 anti-pan-erk

Schema {🗺️}

WebPage:
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         headline:Curcumin synergizes with resveratrol to stimulate the MAPK signaling pathway in human articular chondrocytes in vitro
         description:The mitogen-activated protein kinase (MAPK) pathway is stimulated in differentiated chondrocytes and is an important signaling cascade for chondrocyte differentiation and survival. Pro-inflammatory cytokines such as interleukin 1β (IL-1β) play important roles in the pathogenesis of osteoarthritis (OA) and rheumatoid arthritis (RA). In this study, we investigated whether curcumin and resveratrol can synergistically inhibit the catabolic effects of IL-1β, specifically the inhibition of the MAPK and subsequent apoptosis in human articular chondrocytes. Chondrocytes were either left untreated or treated with 10 ng/ml IL-1β or 1 μM U0126, a specific inhibitor of MAPK pathway alone for the indicated time periods or pre-treated with 10 μM curcumin, 10 μM resveratrol or 10 μM resveratrol and 10 μM curcumin for 4 h followed by co-treatment with 10 ng/ml IL-1β or 1 μM U0126 and 10 μM resveratrol, 10 μM curcumin or 10 μM resveratrol and 10 μM curcumin for the indicated time periods. Cultures were evaluated by immunoblotting and transmission electron microscopy. Incubation of chondrocytes with IL-1β resulted in induction of apoptosis, downregulation of β1-integrins and the extracellular signal-regulated kinase 1/2 (Erk1/2). Interestingly, U0126 induced apoptosis and blocked the above-mentioned proteins in a similar way to IL-1β. Furthermore, curcumin and resveratrol inhibited IL-1β- or U0126-induced apoptosis and downregulation of β1-integrins and Erk1/2 in human articular chondrocytes. These results suggest that combining these two natural compounds activates MEK/Erk signaling, a pathway that is involved in the maintenance of chondrocyte differentiation and survival.
         datePublished:2010-05-25T00:00:00Z
         dateModified:2010-05-25T00:00:00Z
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      headline:Curcumin synergizes with resveratrol to stimulate the MAPK signaling pathway in human articular chondrocytes in vitro
      description:The mitogen-activated protein kinase (MAPK) pathway is stimulated in differentiated chondrocytes and is an important signaling cascade for chondrocyte differentiation and survival. Pro-inflammatory cytokines such as interleukin 1β (IL-1β) play important roles in the pathogenesis of osteoarthritis (OA) and rheumatoid arthritis (RA). In this study, we investigated whether curcumin and resveratrol can synergistically inhibit the catabolic effects of IL-1β, specifically the inhibition of the MAPK and subsequent apoptosis in human articular chondrocytes. Chondrocytes were either left untreated or treated with 10 ng/ml IL-1β or 1 μM U0126, a specific inhibitor of MAPK pathway alone for the indicated time periods or pre-treated with 10 μM curcumin, 10 μM resveratrol or 10 μM resveratrol and 10 μM curcumin for 4 h followed by co-treatment with 10 ng/ml IL-1β or 1 μM U0126 and 10 μM resveratrol, 10 μM curcumin or 10 μM resveratrol and 10 μM curcumin for the indicated time periods. Cultures were evaluated by immunoblotting and transmission electron microscopy. Incubation of chondrocytes with IL-1β resulted in induction of apoptosis, downregulation of β1-integrins and the extracellular signal-regulated kinase 1/2 (Erk1/2). Interestingly, U0126 induced apoptosis and blocked the above-mentioned proteins in a similar way to IL-1β. Furthermore, curcumin and resveratrol inhibited IL-1β- or U0126-induced apoptosis and downregulation of β1-integrins and Erk1/2 in human articular chondrocytes. These results suggest that combining these two natural compounds activates MEK/Erk signaling, a pathway that is involved in the maintenance of chondrocyte differentiation and survival.
      datePublished:2010-05-25T00:00:00Z
      dateModified:2010-05-25T00:00:00Z
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         Chondrocyte
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         Integrins
         OsteoArthritis
         IL-1β
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         Human Genetics
         Clinical Nutrition
         Gene Function
         Biomedicine
         general
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      name:Musculoskeletal Research Group, Institute of Anatomy, Ludwig-Maximilians-University Munich, Munich, Germany

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