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Related Experiment Video

Updated: Jun 18, 2026

Characterization of Thymus-dependent and Thymus-independent Immunoglobulin Isotype Responses in Mice Using Enzyme-linked Immunosorbent Assay
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Characterization of Thymus-dependent and Thymus-independent Immunoglobulin Isotype Responses in Mice Using Enzyme-linked Immunosorbent Assay

Published on: September 7, 2018

Triptolide induces anti-inflammatory cellular responses.

Ranyia Matta, Xianxi Wang, Hui Ge

    American Journal of Translational Research
    |December 4, 2009
    PubMed
    Summary
    This summary is machine-generated.

    Triptolide, derived from Tripterygium wilfordii, significantly inhibits pro-inflammatory gene expression in macrophages. This compound effectively reduces key inflammatory cytokines and microRNA-155, offering insight into the herb

    Keywords:
    Chinese medicineInflammationTripterygium wilfordiicytokinesrheumatoid arthritistranscription

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    Characterization of Thymus-dependent and Thymus-independent Immunoglobulin Isotype Responses in Mice Using Enzyme-linked Immunosorbent Assay
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    Published on: August 11, 2018

    Area of Science:

    • Immunology
    • Molecular Biology
    • Pharmacology

    Background:

    • Tripterygium wilfordii Hook F. is a traditional Chinese medicine used for rheumatoid arthritis.
    • Rheumatoid arthritis involves increased pro-inflammatory cytokine production, such as tumor necrosis factor (TNF)-alpha.
    • Triptolide, purified from T. wilfordii, exhibits potent anti-inflammatory and immunosuppressive properties.

    Purpose of the Study:

    • To investigate the effects of triptolide on global gene expression patterns in lipopolysaccharide (LPS)-stimulated macrophages.
    • To identify specific genes and pathways regulated by triptolide in the context of inflammation.
    • To elucidate the therapeutic mechanisms of T. wilfordii in treating inflammatory conditions.

    Main Methods:

    • Global gene expression analysis using cDNA arrays on LPS-treated macrophages with and without triptolide.
    • Validation of gene expression changes through dose-dependent experiments.
    • Investigation of the effects of triptolide on key signaling pathways, including NF-kappaB and IkappaBalpha phosphorylation/degradation.

    Main Results:

    • LPS stimulation induced 117 genes, with triptolide inhibiting over 50% of these.
    • Triptolide significantly suppressed pro-inflammatory cytokine and chemokine genes (e.g., TNF-alpha, IL-1beta, IL-6) and micro-RNA-155 (miR-155) precursor BIC.
    • Inhibition occurred in a dose-dependent manner, with profound effects at 10-50 nM, and triptolide affected transcription factors beyond NF-kappaB.

    Conclusions:

    • Triptolide potently inhibits the expression of key pro-inflammatory mediators and miR-155 in macrophages.
    • The anti-inflammatory effects of triptolide are not solely mediated by the canonical NF-kappaB pathway.
    • This study provides a molecular basis for the traditional use of T. wilfordii Hook F. in treating inflammatory diseases.