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  2. Matching Content Categories
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We are analyzing https://link.springer.com/article/10.1007/s00210-025-03872-y.

Title:
Dioscin alleviates the dysfunction of fibroblast-like synoviocytes by circ_0008267/miR-942-5p/FKBP5 axis during rheumatoid arthritis | Naunyn-Schmiedeberg's Archives of Pharmacology
Description:
Dioscin is a natural, bioactive steroid saponin that has the antiarthritic activity. Circular RNAs (circRNAs) are stable noncoding RNAs involving in the pathogenesis of rheumatoid arthritis (RA). Here, this study aimed to probe the role and mechanism of dioscin and circ_0008267 in RA progression. Cell proliferation, apoptosis, invasive, and migratory abilities, as well as inflammatory response were evaluated by CCK-8 assay, EdU assay, flow cytometery, transwell assay, wound healing assay, and ELISA analysis, respectively. Levels of genes and protein were tested by qRT-PCR and western blotting. The interaction between miR-942-5p and circ_0008267 or FK506-binding protein 5 (FKBP5) was confirmed using dual-luciferase reporter and RNA pull-down assays. Dioscin treatment was demonstrated to suppress RA-FLS proliferation, invasion, migration, and inflammatory response, but induced cell apoptosis. Circ_0008267 is a stable circRNA, and was increased in RA samples. Moreover, its expression was reduced by dioscin in RA-FLS, overexpression of circ_0008267 reversed the effects of dioscin on RA-FLS. Mechanistically, circ_0008267 acted as a sponge for miR-942-5p, which targeted FKBP5. Dioscin reduced FKBP5 expression, but elevated miR-942-5p level in RA-FLS. MiR-942-5p inhibition or FKBP5 upregulation abolished the inhibitory effects of dioscin on RA-FLS dysfunction. Moreover, circ_0008267 deficiency impaired RA-FLS proliferation, invasion, migration, and inflammation through regulating FKBP5. Dioscin suppressed the proliferation, invasion, migration, and inflammatory response in RA-FLS via circ_0008267/miR-942-5p/FKBP5 axis, providing new insights for RA prevention.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,643,078 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We see no obvious way the site makes money.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {πŸ”}

pubmed, google, scholar, cas, arthritis, dioscin, rheumatoid, central, article, circ, wang, rafls, inflammation, fibroblastlike, axis, proliferation, fkbp, migration, data, synoviocytes, chen, invasion, access, yang, liu, zhang, rnas, cell, mirp, pharmacol, privacy, cookies, content, research, search, circmirpfkbp, natural, study, apoptosis, inflammatory, effects, inhibits, res, nature, authors, springer, information, publish, dysfunction, manuscript,

Topics {βœ’οΈ}

mir-6089/akt1/nf-ΞΊb axis targeting mir-431-5p/fstl1 axis circ_0008267/mir-942-5p/fkbp5 axis circ_0008267/mir-942-5p/fkbp5 forms month download article/chapter elevated mir-942-5p level mir-204-5p-dependent regulation collagen-induced arthritis mice serum lncrna itgb2-as1 mir-766/fkbp5 axis suppress ra-fls proliferation hao xia analyzed central theater command yujing zhang designed mir-942-5p inhibition targeting circular rnas privacy choices/manage cookies circ_0000479 promotes proliferation article naunyn-schmiedeberg' hidden rna language el-sawalhi mm lifeng chen wrote gouty arthritis based full article pdf fkbp5 upregulation abolished rheumatoid arthritis fibroblast rna-based medicines rna-based therapeutics ra progression mir-942-5p holds exclusive rights potential drug targets european economic area bioactive steroid saponin dual-luciferase reporter selective jak3/stat1 efficient microrna sponges h-nmr spectroscopy standardised dioscorea extract rhizoma dioscoreae nipponicae p38 mapk pathway cul4b/wnt pathway updated clinical studies induced cell apoptosis accepted manuscript version conditions privacy policy ra-fls dysfunction dioscin suppressed proliferation check access instant access

Questions {❓}

  • Salmena L, Poliseno L, Tay Y, Kats L, Pandolfi PP (2011) A ceRNA hypothesis: the Rosetta Stone of a hidden RNA language?

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:Dioscin alleviates the dysfunction of fibroblast-like synoviocytes by circ_0008267/miR-942-5p/FKBP5 axis during rheumatoid arthritis
         description:Dioscin is a natural, bioactive steroid saponin that has the antiarthritic activity. Circular RNAs (circRNAs) are stable noncoding RNAs involving in the pathogenesis of rheumatoid arthritis (RA). Here, this study aimed to probe the role and mechanism of dioscin and circ_0008267 in RA progression. Cell proliferation, apoptosis, invasive, and migratory abilities, as well as inflammatory response were evaluated by CCK-8 assay, EdU assay, flow cytometery, transwell assay, wound healing assay, and ELISA analysis, respectively. Levels of genes and protein were tested by qRT-PCR and western blotting. The interaction between miR-942-5p and circ_0008267 or FK506-binding protein 5 (FKBP5) was confirmed using dual-luciferase reporter and RNA pull-down assays. Dioscin treatment was demonstrated to suppress RA-FLS proliferation, invasion, migration, and inflammatory response, but induced cell apoptosis. Circ_0008267 is a stable circRNA, and was increased in RA samples. Moreover, its expression was reduced by dioscin in RA-FLS, overexpression of circ_0008267 reversed the effects of dioscin on RA-FLS. Mechanistically, circ_0008267 acted as a sponge for miR-942-5p, which targeted FKBP5. Dioscin reduced FKBP5 expression, but elevated miR-942-5p level in RA-FLS. MiR-942-5p inhibition or FKBP5 upregulation abolished the inhibitory effects of dioscin on RA-FLS dysfunction. Moreover, circ_0008267 deficiency impaired RA-FLS proliferation, invasion, migration, and inflammation through regulating FKBP5. Dioscin suppressed the proliferation, invasion, migration, and inflammatory response in RA-FLS via circ_0008267/miR-942-5p/FKBP5 axis, providing new insights for RA prevention.
         datePublished:2025-03-21T00:00:00Z
         dateModified:2025-03-21T00:00:00Z
         pageStart:1
         pageEnd:12
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            Pharmacology/Toxicology
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      headline:Dioscin alleviates the dysfunction of fibroblast-like synoviocytes by circ_0008267/miR-942-5p/FKBP5 axis during rheumatoid arthritis
      description:Dioscin is a natural, bioactive steroid saponin that has the antiarthritic activity. Circular RNAs (circRNAs) are stable noncoding RNAs involving in the pathogenesis of rheumatoid arthritis (RA). Here, this study aimed to probe the role and mechanism of dioscin and circ_0008267 in RA progression. Cell proliferation, apoptosis, invasive, and migratory abilities, as well as inflammatory response were evaluated by CCK-8 assay, EdU assay, flow cytometery, transwell assay, wound healing assay, and ELISA analysis, respectively. Levels of genes and protein were tested by qRT-PCR and western blotting. The interaction between miR-942-5p and circ_0008267 or FK506-binding protein 5 (FKBP5) was confirmed using dual-luciferase reporter and RNA pull-down assays. Dioscin treatment was demonstrated to suppress RA-FLS proliferation, invasion, migration, and inflammatory response, but induced cell apoptosis. Circ_0008267 is a stable circRNA, and was increased in RA samples. Moreover, its expression was reduced by dioscin in RA-FLS, overexpression of circ_0008267 reversed the effects of dioscin on RA-FLS. Mechanistically, circ_0008267 acted as a sponge for miR-942-5p, which targeted FKBP5. Dioscin reduced FKBP5 expression, but elevated miR-942-5p level in RA-FLS. MiR-942-5p inhibition or FKBP5 upregulation abolished the inhibitory effects of dioscin on RA-FLS dysfunction. Moreover, circ_0008267 deficiency impaired RA-FLS proliferation, invasion, migration, and inflammation through regulating FKBP5. Dioscin suppressed the proliferation, invasion, migration, and inflammatory response in RA-FLS via circ_0008267/miR-942-5p/FKBP5 axis, providing new insights for RA prevention.
      datePublished:2025-03-21T00:00:00Z
      dateModified:2025-03-21T00:00:00Z
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      pageEnd:12
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         FLS
         Rheumatoid arthritis
         Circ_0008267
         MiR-942-5p
         FKBP5
         Dioscin
         Pharmacology/Toxicology
         Neurosciences
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                  address:
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            name:Yujing Zhang
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                     name:Department of Rheumatology, General Hospital of Central Theater Command, Wuhan, China
                     type:PostalAddress
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      address:
         name:Department of Rheumatology, General Hospital of Central Theater Command, Wuhan, China
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               type:PostalAddress
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      email:[email protected]
      name:Li Xu
      affiliation:
            name:Guiqian International General Hospital
            address:
               name:Department of Cardiovascular Medicine, Guiqian International General Hospital, Guiyang City, China
               type:PostalAddress
            type:Organization
      name:Yujing Zhang
      affiliation:
            name:General Hospital of Central Theater Command
            address:
               name:Department of Rheumatology, General Hospital of Central Theater Command, Wuhan, China
               type:PostalAddress
            type:Organization
      name:Hao Xia
      affiliation:
            name:Medical College of Wuhan University of Science and Technology
            address:
               name:Medical College of Wuhan University of Science and Technology, Wuhan, China
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      name:Department of Rheumatology, General Hospital of Central Theater Command, Wuhan, China
      name:Department of Cardiovascular Medicine, Guiqian International General Hospital, Guiyang City, China
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      name:Medical College of Wuhan University of Science and Technology, Wuhan, China
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